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Constantly updated health news across a range of subjects.
Updated: 13 hours 33 min ago

Broccoli compounds may help combat chronic diseases

Fri, 24/06/2016 - 16:30

"Eating broccoli could lower your risk of having coronary heart disease, type 2 diabetes and several types of cancer, a new study suggests," the Daily Mail reports.

But there is little hard evidence to back up this claim – the study it reports on involved plants, not humans.

Phenols, which are compounds found in broccoli and other cruciferous vegetables, have been linked for years to a lower risk of heart disease, certain cancers, type 2 diabetes and asthma.

They are thought to play a part in reducing oxidative stress – cell damage caused at the molecular level – and inflammation in cells, although the way they do this is unclear.

Because of their potential health-giving properties, plant scientists would like to produce fruits and vegetables with higher levels of phenols.

This study looked at a type of broccoli bred specifically for high phenol content, and mapped which genes and gene sequences were most consistently linked to high phenol production.

However, the study also showed variation between the levels of phenol in different growing conditions, across different years. That suggests it's not as simple as tweaking genes – environmental factors also influence phenol content.

Despite the Mail's headline to the contrary, no type of "genetically tweaked" broccoli has been tested on animals, let alone humans.

Broccoli and other types of green vegetables are recommended as part of a healthy diet, but this study does not provide evidence the vegetable directly reduces the risk of these chronic diseases.  

Where did the story come from?

The study was carried out by researchers from the University of Illinois and the International Institute of Tropical Agriculture in Tanzania, and was funded by the Hatch Multistate Project.

It was published in the peer-reviewed journal, Molecular Breeding.

The Mail focuses on the old news that phenols in broccoli are linked to a lower risk of certain diseases, which was first reported in studies during the 1990s and 2000s.

The reporting is confused and poorly focused. The point of the new study – the researchers' hopes they may be able to breed vegetables with higher levels of phenols – is mentioned, but not in the headline or first few paragraphs.

The fact that this story seems to champion the idea of genetically enhanced broccoli also seems at odds with the newspaper's often-stated editorial policy against so-called "Frankenstein foods": genetically modified, or GM, foods.

What kind of research was this?

This is a plant-breeding study that used molecular and genetic markers to identify certain traits.

The potential health benefits of phenolic compounds found in fruit and vegetables have been extensively studied.

The biological pathways involved in the production of phenols within plants are also quite well understood.

This study aimed to better understand the genetics associated with the production of the highest phenol levels, as well as the environmental factors that could influence this.

The ultimate aim is to breed plants that could be most beneficial for human health.    

What did the research involve?

Researchers crossed two types of broccoli – one alabrese-type and one black broccoli, both of which had high levels of phenols – to create a new hybrid.

They grew it from seed on three different years in different states. During the growing season, they harvested broccoli florets at different points in the plant's growth, freeze-dried and ground them, then used chemical tests to determine their levels of phenols.

The researchers had bred the experimental broccoli with genetic markers, so they could map specific "candidate genes" to see which were most consistently associated with plants that had higher levels of phenols.

They then analysed the results to see what patterns emerged from the interplay of environment and genes.

What were the basic results?

In brief, the researchers found phenol levels varied in the broccoli both within the same year and between different years, suggesting that factors such as the amount of light and the temperature affected the plants' phenol production.

They also identified three candidate genes that played a key role in the early stages of phenol production, which occurred consistently across different years and growing environments.

How did the researchers interpret the results?

The researchers said the results showed that "both genetic and environmental factors play a significant role" in the amount of phenol produced by a plant.

They say the "complex regulatory network" of factors that affect whether specific genes activate phenol production "may at first glance appear to hinder the ability of breeders or growers to enhance phenolic compound accumulation".

However, they go on to say similar work with tomatoes show it may be possible.

They admit that "substantial environmental effects … are a challenge", but suggest that controlled environments such as greenhouses may enable growers to target optimal conditions for growing phenol-rich vegetables.


The "news" that broccoli may protect against some types of disease because they have high levels of phenol compounds is nothing new. We've known about the link between diets rich in phenolic compounds and the lower risk of heart disease since 1995.

This study looks instead at the mechanisms within broccoli plants that regulate how much phenol a plant produces.

Perhaps unsurprisingly, this varies a lot and seems to be affected both by the plant's genetic make-up and the environmental conditions in which it is grown.

The research may help food growers to increase the amount of phenol compounds in vegetables – including veg other than broccoli – using breeding programmes, genetic modification or controlled growing conditions, such as greenhouses.

However, this research is just one step on the pathway to that. More research will be needed to put these tentative findings into practice.

Also, this study does not involve people and in itself provides no direct evidence that eating large amounts of broccoli – high phenolic or otherwise – will directly influence your risk of cancer, heart disease, diabetes or any other chronic diseases.

Anyone wanting to increase the phenol content in their diet can do so by eating not just broccoli, but many other fruits and vegetables, including green vegetables, tomatoes, beans, berries and stone fruits.

Better still, why not try growing some in your garden or allotment? For more info, read some tips for growing your own fruit and vegetables

Links To The Headlines

Why broccoli really IS a superfood: Compounds in the veg lower the risk of cancer, heart disease and diabetes. Daily Mail, June 24 2016

Links To Science

Gardner AM, Brown AF, Juvik JA. QTL analysis for the identification of candidate genes controlling phenolic compound accumulation in broccoli (Brassica oleracea L. var. italica). Molecular Breeding. Published online June 11 2016

Categories: NHS Choices

Study suggests that inflammation is behind period pain

Thu, 23/06/2016 - 14:00

"Scientists have finally discovered why periods hurt so much, following a ground-breaking study into menstrual pain," The Independent reports.

A new study suggests that the pain is caused by acute inflammation, as measured by the C-reactive protein (CRP). CRP is a protein produced by the liver; its levels rise when there is inflammation present in the body.

In this latest research, scientists wanted to see if raised levels of CRP were associated with the often reported feelings of dull painful cramping many women feel before their period. This symptom is a common occurrence in what is known as premenstrual syndrome (PMS).

PMS is the name given to the pattern of physical, psychological and behavioural symptoms that can occur two weeks before a woman's monthly period.

Overall, the study found that middle-aged women with raised CRP levels had about a 26-41% increase in risk of the various PMS symptoms. However, it is difficult to prove direct cause and effect between these two things and exclude the influence of other factors. The findings may also not apply to girls and younger women with PMS.

The authors hope that these results will pave the way for future research into therapeutic treatments for PMS. While not life-threatening, PMS can cause a considerable negative impact on quality of life.

Taking steps to avoid factors associated with increased inflammation – such as smoking, overweight and obesity – may also help.


Where did the story come from?

The US study was carried out by researchers from the University of California, Davis, and was funded by grants from the National Institutes of Health (NIH), the National Institute on Aging (NIA), the National Institute of Nursing Research (NINR), and the NIH Office of Research on Women's Health (ORWH).

The study was published in the peer-reviewed medical publication Journal of Women's Health. It is available on an open-access basis and can be read for free online.

The Independent was slightly pre-emptive when reporting that, "a ground-breaking study has found a link between inflammation and PMS". This alleged link cannot be confirmed from the methodology used in this research, which was a cross-sectional analysis. However, the main body of the article was accurate.


What kind of research was this?

This was a cross-sectional analysis of data taken from a long-running cohort study being carried out in the US. It aimed to investigate whether CRP levels (C-Reactive Protein – a blood inflammatory marker) were associated with premenstrual symptoms.

Around 80% of women suffer from PMS and 50% seek medical advice for them, placing a sizeable burden on the healthcare system.

Cross-sectional studies like this are useful in assessing the incidence and prevalence of medical conditions or health indicators, but they are unable to prove causation, and say, for example, that raised inflammatory markers/inflammation cause the symptoms. It's probably more of a complex relationship that could involve other factors. A prospective cohort study would be one of the best ways to validate these findings.


What did the research involve?

The data for this analysis was obtained from the Study of Women's Health Across the Nation (SWAN), which is a longitudinal study of midlife women in the US. SWAN is currently following a cohort of 3,302 women from five ethnic groups at seven clinical institutions across the nation – it continues to collect data on reproductive health, plus demographic and lifestyle factors, through self-reported questionnaires.

As part of the initial questionnaire, participants were asked about their periods and to indicate a yes/no response to eight commonly reported premenstrual symptoms:

  • abdominal cramps/pain
  • breast pain/tenderness
  • weight gain/bloating
  • mood changes/suddenly sad
  • increase in appetite or craving
  • feeling anxious/jittery/nervous
  • back/joint/muscle pain
  • severe headaches

Blood CRP levels were also measured.

This cross-sectional analysis used the data from the baseline visit (in 1996/97) to assess whether CRP levels were associated with pre-menstrual symptoms. Participants were included in the analysis if they were aged 42-52 before or around the time of the menopause, had not undergone a hysterectomy or had both ovaries removed, were not pregnant, and were not using hormone replacement therapy or oral contraceptives at baseline. CRP-levels were categorised into "elevated" (>3mg/L) and "non-elevated" (≤3mg/L) for the analysis.

Other potential risk factors were controlled for to assess the true effect of CRP levels on PMS symptoms. This study included 2,939 women from the original cohort with full data available.


What were the basic results?

Overall, elevated CRP levels (>3mg/L) were significantly related to a 26-41% increased odds of reporting PMS symptoms. However, this relationship varied between different symptoms, suggesting that other mechanisms may be responsible for the occurrence of different symptoms.

The analysis also found that symptoms were reported more by Hispanic women and those around the time of the menopause, and significantly less in Chinese and Japanese individuals, compared to Caucasian or premenopausal women. A higher education (more than high school) and higher annual income were associated with fewer PMS symptoms.

Most symptoms were reported significantly more by obese women, those with active or passive smoke exposure, and women with elevated depressive symptoms.


How did the researchers interpret the results?

The researchers concluded: "These results suggest that inflammation may play a mechanistic role in most PMS symptoms, although further longitudinal study of these relationships is needed. However, recommending to women to avoid behaviours that are associated with inflammation may be helpful for prevention, and anti-inflammatory agents may be useful for treatment of these symptoms."



This study found that middle-aged women with elevated CRP levels were more likely to report symptoms of PMS.

The study had a good sample size, and represented a racially diverse and community-based sample of women who could be generalised to the US population of middle-aged women.

However, there are a few points to bear in mind:

  • It is unclear whether CRP levels were measured two weeks before a woman's period, so the results may differ, depending on the stage of the menstrual cycle.
  • As the researchers acknowledge, some of the associations observed may have resulted from other exposures, such as anti-inflammatory medications, physical activity and depressive symptoms.
  • It is difficult to imply the direction of effect/causation. A longitudinal study would be needed to better assess whether a rise in CRP levels preceded the onset of PMS, or vice versa.
  • No information was collected on the presence of infection in participants, which could have influenced the increased levels of inflammation.
  • Lastly, the findings cannot be applied to girls or younger women. It is also possible that PMS prevalence and associations could differ between women of different cultures and ethnicities than the US population sampled in this study.

The researchers hope that these results will pave the way for future research, as well as potential therapeutic treatments for PMS symptoms through advice about avoidable factors associated with increased inflammation, such as smoking, overweight and obesity.

Usually, a step-wise approach is recommended for PMS. Women with mild symptoms can usually relieve symptoms using over-the-counter painkillers and self-care techniques, such as eating smaller meals more frequently to help reduce bloating.

Women with more severe symptoms should see their GP, as they may benefit from the use of prescription medication.

Read about the treatment options for PMS symptoms.

Links To The Headlines

Period pain: Scientists finally work out why menstruation hurts so much. The Independent, June 21 2016

Links To Science

Gold EB, Wells C, Rasor MO. The Association of Inflammation with Premenstrual Symptoms. The Journal of Women’s Health. Published online  May 2016

Categories: NHS Choices

Should we 'eat breakfast like a king and dinner like a pauper'?

Thu, 23/06/2016 - 13:00

"We should 'eat breakfast like a king' to fight obesity, scientists claim," the Daily Mirror reports.

The headline was prompted by a new review into "chrono-nutrition", which involves seeing if when we eat is as important as what we eat.

The review suggests eating more of our total daily food intake in the evening – the pattern most common among people in the UK – may be linked to obesity.

But the evidence for this is not conclusive, and the studies included in the review vary in their findings.

The study also shows there is a wide variation in the eating patterns of people in different countries.

Previous research found eating breakfast is linked to a lower risk of obesity, supporting the theory that it's better to eat earlier than later.

However, this study's authors say we are still a long way off understanding the optimum eating patterns for health.

One note of caution is that the methods used in this review are poorly described and not what you would expect to see from a comprehensive systematic review. This means it's possible the authors have not considered all literature relevant to the issue.

Current dietary advice is not to skip your morning meal and to eat a healthy, balanced breakfast with plenty of wholemeal, vegetables, fruit and limited saturated fat, sugar and salt.

Where did the story come from?

The study was carried out by researchers from Imperial College London, Nestlé Research Centre, the University of Thessaly, King's College London, and VU University Amsterdam. 

The authors report no funding and no conflicts of interest. However, Nestlé produces breakfast cereals, so the company is likely to have an interest in this type of research.  

The study was published in the peer-reviewed Proceedings of the Nutrition Society on an open-access basis, so it is free to access online.

Both The Daily Telegraph and the Mirror plumped for the "Eat breakfast like a king, lunch like a prince and dinner like a pauper" adage in their headlines.

However, they don't make it clear that the study's findings are uncertain and require more – and better – research before they can be confirmed.

What scientist Dr Gerda Pot actually said was: "There seems to be some truth in the saying 'Eat breakfast like a king, lunch like a prince and dinner like a pauper'; however, this warrants further investigation." 

What kind of research was this?

This was a review of observational studies, including cross-sectional surveys and longitudinal cohort studies.

It aimed to look at global trends in timing of food intake and see how this could be linked to obesity.

systematic review is a good way to get an overview of research in a field.

However, observational studies can only tell us about a link between factors – in this case, whether obesity is linked to eating at particular times of day – and not whether one factor causes another.

Notably in this case, however, the methods the researchers used are not outlined in full, so it cannot be said with any degree of certainty that this is a fully comprehensive systematic review of the relevant literature. 

What did the research involve?

Researchers reviewed studies looking at people's energy intake at different times during the day, and identified common eating patterns in different countries.

They also reviewed studies that looked at the association between the time of day someone eats and obesity or weight. They then summarised the findings.

The researchers aimed to only include studies that used standardised dietary questionnaires. Even so, there was much variation in the way eating patterns were described.

They excluded studies that looked at very specific groups – for example, athletes or people being treated for specific medical conditions.

Most studies divided eating times into four groups: breakfast, lunch, dinner and snacks. But in most cases there was no information about when people ate snacks.

Although the authors described their general study inclusion and exclusion criteria, they did not clearly set out their methods in the way you would expect from a systematic review.

For example, they did not give information on which literature databases they searched, the search dates, search terms, or a description of how studies were quality-assessed for inclusion.  

What were the basic results?

Researchers identified four main patterns of food consumption, seen in 11 studies from different countries:

  • equal energy consumption at breakfast and dinner, with the greatest consumption at lunch – seen in Guatemala and Poland
  • smallest energy consumption at breakfast, greatest consumption at lunch, followed by dinner – seen in France, Switzerland and Italy
  • equal energy consumption at breakfast and dinner, with the smallest consumption at lunch – seen in Sweden
  • smallest consumption at breakfast, greater consumption at lunch, and greatest consumption at dinner – seen in the UK, the US, Germany, Canada, Denmark, the Netherlands and Belgium

They included 10 studies that looked at the link between eating, time of day and weight.

The studies used a variety of methods to assess the link, differing numbers of days of assessment, and different outcome measures, including different ways of reporting body mass index (BMI) and fat distribution.

This makes it hard to summarise, but the key findings from the studies were:

  • one study found people who ate more in the evening, compared with the morning, were likely to have a higher BMI
  • one study found eating between meals was linked to more body fat
  • one study found people who didn't eat breakfast ate more later in the day and had a higher BMI
How did the researchers interpret the results?

The researchers said: "On the balance of this evidence, it could be speculated that evening energy intake is a major risk factor for obesity", but they go on to add that more study data is needed to confirm this.

They warn of difficulties in drawing conclusions from the studies they found, which varied widely in their methods, and say researchers need to reach agreement on how to define eating patterns, and future studies should record the timing of snacks.

They also say the data in the review "might not summarise current trends" because it does not include currently ongoing national studies.


This study gives a fascinating overview of the different ways people from different cultures eat.

It also includes interesting historical information – for example, breakfast was considered sinful in medieval England, while 10th-century Middle Eastern doctors recommended eating two meals a day, before dawn and at dusk.

But what it cannot do is tell us which eating patterns are healthiest to provide the best energy intake distribution throughout the day for our modern lives.

The evidence linking obesity with evening energy intake is interesting, but there is not enough good-quality data to rely on this finding.

Also, confounding health and lifestyle factors could contribute to this link – for example, people who eat less in the evening might do so because they are out at the gym, rather than sitting in front of the television.

The paper also points to the cultural context of eating as being likely to affect when we eat, as well as what we eat.

For example, in France – where lunch is the biggest meal of the day – people are more likely to sit down to a full meal at lunchtime, perhaps in family groups.

In the UK, food consumption is more individual and informal – perhaps a sandwich and bag of crisps at the desk at lunchtime, or an evening takeaway.

A second study in the same publication found eating irregularly, rather than at regular meal times, may be linked to the chances of getting diabetes. We were unable to see the full study, so we cannot assess the evidence for this.

We cannot be sure this is a comprehensive review of all literature relevant to this issue. Again, many of the elements of the methods you would expect to see recorded in a well-conducted systematic review are missing.

This means it is possible the researchers may not be presenting a fully impartial review of this subject, and some relevant studies could be missing.  

There is no official advice in the UK about when we should have our meals, although people are advised not to skip breakfast.

Read more about healthy eating.

Links To The Headlines

We should 'eat breakfast like a king, lunch like a prince and dinner like a pauper' to fight obesity, scientists claim. Daily Mirror, June 22 2016

Breakfast like a king, lunch like a prince and dine like a pauper to stay healthy, say scientists. The Daily Telegraph, June 22 2016

Links To Science

Almoosawi S, Vingeliene S, Karagounis LG, Pot GK. Chrono-nutrition: a review of current evidence from observational studies on global trends in time-of-day of energy intake and its association with obesity. Proceedings of the Nutrition Society. Published online June 22 2016

Categories: NHS Choices

Diabetes drugs may be useful for Alzheimer's, mice research finds

Wed, 22/06/2016 - 16:30

"Drugs prescribed to treat diabetes could cure Alzheimer's disease" is the significantly over-hyped headline in The Daily Telegraph.

What this new research actually found is that there seem to be shared biological processes between Alzheimer's and diabetes. But the study concerned did not look at treatments for the disease, never mind any possible cures.

The report highlights a study in genetically engineered mice concerning a human enzyme (BACE1) that is closely linked to the development of Alzheimer's disease in humans, and which recent studies have also shown could be linked to type 2 diabetes. This study supported this concept, finding that mice bred to produce BACE1 showed signs of poor glucose control when compared with "normal" mice.

Research has previously linked diabetes with the risk of getting Alzheimer's disease. Researchers now suspect the link also works the other way round, so people with Alzheimer's disease may be more likely to get diabetes after getting dementia.

This animal study therefore looked at potential mechanisms that might affect the development of both diseases. However, the findings may not necessarily translate to humans. It has not tested the effects of diabetes drugs on the signs and symptoms of Alzheimer's, or vice versa.

Much more research is needed. Talk of a treatment or cure for Alzheimer's is premature and risks getting people's hopes up unfairly.

Maintaining a healthy weight and eating a nutritious diet can reduce both the risks of type 2 diabetes and Alzheimer's, but as of yet, there is no guaranteed method to prevent Alzheimer's disease.


Where did the story come from?

The study was carried out by researchers from the University of Aberdeen and the University of the Highlands and Islands, and was funded by a variety of grants and fellowships from organisations including Romex Oilfield Chemicals, Scottish Alzheimer's Research UK, the University of Aberdeen, the British Heart Foundation, Diabetes UK and Study of Diabetes/Lilly.

The study was published in the peer-reviewed journal Diabetologia on an open-access basis, so it is free to read online.

The UK media seems to have jumped the gun, from a study that looks at complex metabolic pathways in genetically modified mice, to reports that diabetes drugs could cure Alzheimer's disease. The Daily Mail probably did the best job of covering it, although the first mention that the study was on mice came some way down the story.

The Daily Telegraph did a poorer job, with a headline that was entirely inappropriate for the implications of the study.


What kind of research was this?

This was an observational laboratory study of mice bred to produce a human enzyme called BACE1. The researchers compared the mice with wild-type ("normal") mice, looking at their glucose control, lipids (fats) and other indicators of diabetes. They wanted to see whether mice bred to produce BACE1 were more likely to show signs of diabetes.

BACE1 is linked to the production of amyloid protein in the brain, which is characteristic of Alzheimer's disease. Recent studies have also shown that a lack of this enzyme could protect against obesity and diabetes, suggesting it may have an influence on glucose regulation in the body.

Animal studies are useful ways of carrying out experiments that cannot be done on humans, but it is not certain that results in animals translate to results in humans or lead to new treatment approaches.


What did the research involve?

Researchers took two groups of mice – one group similar to mice found in the wild, and the other bred to express a human enzyme called BACE1 in their brain cells. They monitored and tested them at three, four, five and eight months of age. They compared the results between the two groups.

The mice had a range of tests, including for glucose tolerance and insulin production, CT scans to look at the amount of fat they had, and tests for a range of markers, including leptin (a hormone linked to hunger), glycogen (the form in which the liver stores glucose) and types of lipids.

The researchers used statistical analysis to compare results between the two groups of mice, taking account of their initial body weight and food consumption.


What were the basic results?

Mice with BACE1 had results similar to wild-type mice until they were about four months old. After that, their weight went down, but the amount of fat in their bodies went up.

Blood tests after four months showed raised glucose levels and progressive raised glucose intolerance, altered levels of hormones and lipids, impaired ability of the liver to store glucose as glycogen, and reduced metabolism of glucose in the brain. All of these results suggest the BACE1 mice were unable to control their glucose levels, which is the major sign of diabetes.

The researchers said their previous research had shown that BACE1 mice begin to show signs of dementia at four to six months of age. They added: "Our current findings therefore indicate that neuronal BACE1 induces global metabolic dysregulation, along with brain inflammation and amyloidosis-related cognitive decline." They say the study "pinpoints neuronal BACE1" as the major driver of the inability to regulate glucose.


How did the researchers interpret the results?

The researchers say they have demonstrated that "neuronal expression of human BACE1 causes systemic diabetic complications."

They say their work "provides insight into the complex mechanistic interactions between diabetes and Alzheimer's disease" and shows that not only does diabetes increase the risk of Alzheimer's disease, but that the reverse may also apply.



Both Alzheimer's disease and diabetes seem to have become more common in recent years, causing illness and putting strain on the health service. News that the two illnesses may have a common cause raises hopes that drugs which help with one disease may also be of use in treating another.

Trials of a diabetes drug on people with Alzheimer's disease are reported to be underway, although no results have been published yet. This study, suggesting a mechanism which may be involved in the early stages of both diseases, may increase the likelihood that common treatments will be useful.

The study's main limitation is that it was carried out on mice, and studies in animals do not always translate directly to people. It's important to realise the study was not looking at ways to cure either diabetes or Alzheimer's disease, but only at an enzyme which may be implicated in the development of both. We don't know exactly what effect it has on humans, or how many people with raised levels of BACE1 get diabetes or Alzheimer's.

Studies like these, carried out on laboratory animals, can play an important role in helping us discover more about diseases and their causes. But we won't know whether this insight will help to find a treatment for Alzheimer's disease until there have been human trials.

If you had been diagnosed with type 2 diabetes, then sticking to your recommended treatment plan, in terms of diet and medication, should help reduce your Alzheimer's risk. Read more about Alzheimer's disease prevention.

Links To The Headlines

Drugs used to treat diabetes could cure Alzheimer's, experts say. The Daily Telegraph, June 21 2016

Scientists discover strong link between diabetes and Alzheimer's: Drugs used to control glucose levels may halt progression of dementia. Mail Online, June 22 2016

The diabetes drug that can also be used to fight off dementia. Daily Mirror, June 21 2016

Links To Science

Plucińska K, Dekeryte R, Koss D, et al. Neuronal human BACE1 knockin induces systemic diabetes in mice. Diabetologia. Published online May 2 2016

Categories: NHS Choices

Drugs, ginger and acupuncture 'best for morning sickness'

Wed, 22/06/2016 - 13:35

"Hundreds of thousands of pregnant women with morning sickness should be given drugs to ease their symptoms," the Daily Mirror reports.

The recommendation comes from a set of new guidelines that also say ginger and acupuncture can play a useful role in treating nausea and vomiting in pregnancy, better known as morning sickness.

Health professionals prefer to call it nausea and vomiting in pregnancy as it can occur at any time, not just in the morning.

The new guidelines (PDF, 545kb) were produced by the Royal College of Obstetricians and Gynaecologists, a UK professional body of clinicians that seeks to improve healthcare for women.

Nausea and vomiting in pregnancy

Nausea and vomiting in pregnancy is very common in early pregnancy, affecting the majority of women in their first trimester.

It's unpleasant, but doesn't place the pregnancy at any increased risk and usually clears up by weeks 16 to 20 of pregnancy.

Hyperemesis gravidarum

The guidelines also discuss hyperemesis gravidarum, where women experience excessive nausea and vomiting.

They might be sick many times a day – some women report being sick up to 50 times a day – and be unable to keep food or drink down.

This is far less common than nausea and vomiting in pregnancy, affecting around 1 in every 100 women.

The Duchess of Cambridge, née Kate Middleton, reportedly suffered from hyperemesis gravidarum during her first pregnancy.

What are the main recommendations?

The main recommendations of the guidelines are outlined below.

Self care

Most women with nausea and vomiting in pregnancy can manage their symptoms themselves using self care techniques.

These include:

  • eating small amounts of food often, rather than having several large meals – but don't stop eating
  • eating cold meals, rather than hot ones, as they don't give off the smell that hot meals often do, which may make you feel sick
  • avoiding foods or smells that make you feel sick
Complementary therapies

The guidelines mention there is some evidence that ginger supplements may help reduce nausea and vomiting.

To date, there have not been any reports of adverse effects being caused by taking ginger during pregnancy.

However, ginger products are unlicensed in the UK, so buy them from a reputable source, such as a pharmacy or supermarket. Check with your pharmacist before you use ginger supplements.

Similarly, acupressure on the wrist may also be effective in reducing symptoms of nausea in pregnancy.

Acupressure, similar to acupuncture, involves wearing a special band or bracelet on your forearm.

The guidelines do not recommend the use of hypnotherapy, as there is no evidence it is effective.


If symptoms fail to respond to these approaches, medication is recommended, which can be prescribed by your GP.

Anti-sickness medications (antiemetics) known to be safe during pregnancy, such as cyclizine, are usually recommended.

Some antihistamines, often used to treat allergies such as hay fever, also work as antiemetics.

Admission to hospital

Admission to hospital may be recommended if you:

  • are dehydrated
  • have severe vomiting and are unable to tolerate any fluids
  • have abnormal blood tests
  • have lost weight
  • have a medical condition, such as a heart or kidney problem, or diabetes
What happens in hospital?

You will be given the fluids you need though a drip in your arm. This will be continued until you are able to drink fluids without vomiting.

You should be offered anti-sickness medication and a B vitamin called thiamine. Both of these can be given through the drip in your arm if you are unable to keep tablets down.

Compression stockings and medications may be used to help prevent blood clots. Being dehydrated and not being mobile increases blood clot risks.

You should be discharged from hospital once your symptoms improve.

Links To The Headlines

Pregnant women with morning sickness should be given drugs to ease symptoms, say doctors. Daily Mirror, June 22 2016

Ginger and acupressure 'options for morning sickness'. BBC News, June 22 2016

All pregnant women suffering morning sickness to be offered drugs rather than 'suffer in silence'. Daily Mail, June 22 2016

Use drugs to help women beat morning sickness, GPs urged. The Times, June 22 2016 (subscription required)

Links To Science

Royal College of Obstetricians and Gynaecologists. The Management of Nausea and Vomiting of Pregnancy and Hyperemesis Gravidarum (Green-top Guideline No.69). June 2016

Categories: NHS Choices

Almost half of all UK adults may be living with chronic pain

Tue, 21/06/2016 - 16:30

"Almost half the adult population is living with chronic pain," the Daily Mail reports. A major new review suggests that around 28 million adults in the UK are affected by some type of chronic pain (pain that lasts for more than three months).

The researchers used data from 19 studies that included almost 140,000 adults. They extrapolated the results to come up with the estimate that around 43% of people in the UK experience chronic pain. More adults aged 75 or over (62%) experienced pain than those aged 18 to 25 (14.3%).

There are limitations to this study that affect the reliability, the main one being that this type of review can only be as good as the included studies. In this case, there weren't many good-quality studies and there was a lot of variation in their findings.

With an ageing population, it is likely that the prevalence of chronic pain will increase and the need for pain management and relief will grow.

A case could be made that health services across the world need to do more to meet the needs of people with chronic pain. While it may not be life-threatening, chronic pain can cause considerable distress and adversely affect mental health.

Current advice for chronic pain is to use a combination of physical exercise and painkillers to relieve pain. Psychological therapies, such as cognitive behavioural therapy, can also help people cope better with quality of life issues.


Where did the story come from?

The study was carried out by researchers from Imperial College London, Arthritis Research UK and the University of Aberdeen. Funding was provided by the British Pain Society and Arthritis Research UK.

Conflict of interest was declared by one of the researchers who had received fees from pharmaceutical companies including Grunenthal, Napp/Mundipharma, Pfizer, Astrazeneca, BioQuiddity and The Medicines Co, outside the submitted work.

The study was published on an open access basis in the peer-reviewed medical journal BMJ Open, so you can read it for free online.

This has been reported widely by the UK media, which generally provided an accurate account of the research findings. However, limitations of the included studies that might reduce reliability were not mentioned. 


What kind of research was this?

This was a systematic review and meta-analysis which aimed to combine existing data on the prevalence of chronic pain in the general population. The researchers investigated various definitions of chronic pain to attempt to provide national estimates.

A systematic review is the best way of combining all available data on a health issue. However, the limitation is that it can only be as reliable as the included studies – if these are of poor quality, then the findings of a systematic review should be interpreted with caution.

Similarly, the results of a meta-analysis may be subject to question if there was a great deal of difference (heterogeneity) between individual studies.


What did the research involve?

The review team searched two medical databases, Medline and Embase, for articles reporting on the prevalence of chronic pain in the general UK population. All study types were included, providing they reported prevalence estimates for the following:

  • chronic pain – pain in one or more locations in the body
  • chronic widespread pain – using the American College of Rheumatology (ACR) definition (1990) of pain in the head or spine and two limbs on opposite side of the body
  • fibromyalgia – ACR criteria (1990 or 2010) of widespread pain and tenderness in many different parts of the body, along with other symptoms of the condition (e.g. lethargy)
  • nerve pain (neuropathic pain) – pain in one or more body locations with nerve features, such as numbness or tingling

Each definition of pain was to be present for at least three months.

The researchers excluded studies containing data prior to 1990, or if it was not representative of the UK population, or it was not possible to retrieve UK-specific estimates. They also excluded studies investigating specific pain sites only (e.g. prevalence of lower back pain only), or studies in specific populations who wouldn't represent the general population (e.g. chronic pain prevalence in people with diabetes).

Two researchers reviewed search results, selected studies which met their criteria, and collected prevalence data.

All included studies were assessed using a risk of bias tool. Studies that had a very high risk of bias were not included in the analysis.

Statistical methods were used to combine the findings of individual studies.


What were the basic results?

The database searches found 1,737 potentially relevant studies. On further examination, only 19 met their inclusion criteria, presenting data from 139,933 adults in the UK. Most of these (13) were cross-sectional studies, and the remainder were cohort studies.

The review found that 43.5% of people experienced chronic pain of some kind (pooled results from seven studies). Prevalence ranged from 35% to 51% in the individual studies. The prevalence of moderate to severely disabling chronic pain was lower and ranged from 10.4% to 14.3% (based on four studies).

The researchers split estimates for chronic pain into age groups and, as you might expect, found a theme for increasing prevalence with increasing age. This ranged from 14.3% in younger adults (18 to 25 years old), to 62% for those over 75 years of age.

Findings using the three other pain definitions were:

  • chronic widespread pain – 14.2% (pooled result from five studies)
  • chronic neuropathic pain – 8.2% to 8.9% (results in two studies)
  • fibromyalgia – 5.4% (one study)
How did the researchers interpret the results?

The researchers conclude: "Chronic pain affects between one-third and one-half of the population of the UK, corresponding to just under 28 million adults, based on data from the best available published studies. This figure is likely to increase further in line with an ageing population."



This systematic review aimed to combine available data on the prevalence of chronic pain in the UK adult population.

The 19 identified studies suggested that 43% of people in the UK experience chronic pain. However, there are both strengths and limitations to this review that may affect the reliability of this finding.

The review has strengths in the careful search methods which aimed to identify only studies relevant to the general population. The researchers also did their best to provide the most reliable estimate by performing a quality assessment of studies and excluding those at particularly high risk of bias.

The main limitation is that a systematic review can only be as good as the included studies, and in this case there were few high-quality studies and a lot of variation in their findings. The included studies mainly collected data using questionnaires, which are subject to various sources of bias.

The response rate ranged from 36.3% to 89.7% and it is possible that those who respond are more likely to be experiencing pain than those who aren't. If this was the case, then this could be an overestimate of prevalence. We also cannot tell from these findings what the cause of pain was, and whether people were receiving the appropriate management for it.

Whether the prevalence found in this review is accurate or not, living with chronic pain has a negative impact on quality of life. It can affect mobility and limit daily activity, affect employment, social and personal life, and affect mental health (e.g. depression). With an ageing population, it is likely that the prevalence will increase and the need for pain management and relief will grow.

There are a number of treatment options available on the NHS for people struggling with chronic pain, such as physiotherapy, pain management courses, and counselling.

Read more on how to get NHS help for your pain.

Links To The Headlines

How half of Britons are suffering from long term pain: Up to 28 million adults in Briton have struggled with discomfort for more than three months. Daily Mail, June 21 2016

Up to half of UK people living in pain. BBC News, June 21 2016

'Silent epidemic' of chronic pain affects nearly 28 million in UK, study suggests. The Guardian, June 21 2016

Nearly half of Britons suffer from chronic pain, study finds. The Daily Telegraph, June 20 2016

Up to 28 million Britons live with chronic pain. The Times, June 21 2016

Links To Science

Fayaz A, Croft P, Langford RM, et al. Prevalence of chronic pain in the UK: a systematic review and meta-analysis of population studies. BMJ Open. Published online June 20 2016

Categories: NHS Choices

Cranberry juice 'useful' for women with recurring UTIs, claims study

Mon, 20/06/2016 - 18:00

"Drinking cranberry juice could reduce the worldwide use of antibiotics," is the somewhat optimistic headline in The Daily Telegraph.

A new study found some modest preventative benefit in women with a history of reoccurring urinary tract infections (UTIs), though this arguably doesn't amount to an effective weapon in the war against antibiotic resistance.

In the interests of transparency, it is important to point out that the study was funded by Ocean Spray Cranberries and two of the authors were employed by the company.

This was a six-week trial in 373 healthy women who drank either a 240ml bottle of cranberry juice or identical-tasting placebo every day for six weeks. It found that cranberry juice reduced the number of symptoms associated with UTIs.

The scale of the preventative effective was modest. The researchers estimated that, on average, for every woman who drank cranberry juice for 3.2 years, just one UTI would be prevented. That's a lot of cranberry juice.

The study had a good sample size, duration of follow-up, regular assessments, and participants and researchers were unaware of the study group. However, it's important to realise that the juice only seemed to reduce the number of infections across the group – not treat them. Women with an actual infection still needed to take antibiotics. The study also excluded people who may be most susceptible to urine infections.

The decision whether to drink daily cranberry juice remains a personal one – but it is worth bearing in mind that these drinks are usually high in sugar.  

Where did the story come from?

The study was published in the peer-reviewed American Journal of Clinical Nutrition. Funding was provided by Ocean Spray Cranberries Inc. which provided the drink used in the study. Two of the study authors work for the firm.

While industry funding for a study is not unusual, actually having authors of a study being employed by a funding company is. While there is no suggestion of obvious bias, the study is vulnerable to accusations of a conflict of interests, due to an unconscious bias on the part of the company's employees.

The study was published on an open access basis, so you can read it for free online.

The Telegraph and The Daily Mail acknowledge the potential conflict of interest inherent in the study, but also suggest that cranberry juice could help combat antibiotic resistance at face value. This seems quite a bold claim, given the modest effects reported in the study.

The Metro takes a more critical approach, citing a number of objections raised by the American news website, Vox, which attacks the methodology of the study.


What kind of research was this?

This was a randomised controlled trial aiming to looking at the effects of drinking cranberry juice on episodes of UTIs in women.

UTIs are common among healthy women, and it is estimated that between a quarter and a third of women who develop an infection will have a recurrent one within the following six months.

Antibiotics are used in the treatment and prevention of UTIs. However, the increasing problem of antibiotic resistance and the side effects of antibiotics make this far from ideal.

Cranberries have often been proposed to have benefits in protecting against UTIs (a claim thought to date back to Native American tradition).

A double-blind placebo-controlled trial such as this is the best way of investigating this theory. 


What did the research involve?

The trial was carried out across 18 clinics in the US and involved 373 healthy women (average age 41) who had suffered two or more UTIs over the past year. Women with a current UTI and those taking preventative antibiotics were excluded.

They were randomised to drink a 240ml bottle of cranberry juice or identical placebo (a flavoured, sugary drink) every day for six months.

Participants kept a daily diary to record any UTI symptoms. They attended planned clinic assessments at two, four and six months, but if they experienced UTI symptoms at any time they contacted the research centre to attend for another assessment.

At assessments, urine samples were collected and tested. The main outcome of interest was the frequency of UTI symptoms. Other outcomes included the incidence of UTI with positive urine test, and side effects.

Throughout the study, participants were asked to avoid cranberries and blueberries or their products, and probiotics, including yoghurt. Compliance was assessed by asking participants to return all used and unused bottles at the end of the study – and was 98%. 322 of the randomised participants (86%) completed the full six-month study.


What were the basic results?

Cranberry juice significantly reduced the incidence of UTIs. During follow-up, there were 39 symptomatic infections in the cranberry group compared with 67 in the placebo group, with an annual incidence of 0.48 vs. 0.75. This meant that cranberry juice reduced the incidence of UTIs by over a third (rate ratio 0.61, 95% confidence interval [CI] 0.41 to 0.91).

With confirmation by urine dipstick, there were 32 infections vs. 53. Adjusting for antibiotic use during UTIs did not significantly affect the results.

Overall, the researchers estimated that cranberry juice would prevent roughly one symptomatic UTI per three women per year ("One clinical UTI event was prevented for every 3.2 woman years").

The only difference in side effects between groups was at two months, when nausea was reportedly more common in the placebo group (5.9% vs. 1.6% of participants in the cranberry group).


How did the researchers interpret the results?

The researchers conclude: "The consumption of a cranberry juice beverage lowered the number of clinical UTI episodes in women with a recent history of UTI".



This trial found that drinking cranberry juice daily for six months reduced the number of symptomatic urine infections among healthy women, compared with placebo.

The study had a good sample size, reasonably long testing period, was double-blind, including reportedly identical tasting-and-smelling placebo. It also carried out thorough assessments, verifying any reported symptoms with urine tests.

However, there are a few points to note.

  • The study found that cranberry juice seemed to prevent the incidence of urine infection symptoms. It does not show that if you have an actual urine infection you are better off just drinking cranberry juice, as it is better or just as good at clearing the infection as antibiotics. Women who developed an infection in this study were still given antibiotic treatment.
  • The study excluded women who needed to take preventative antibiotics and others who may be at a higher risk of UTIs, such as those with indwelling catheters, any problems or abnormalities of the urinary tract, those with sensory problems (e.g. spinal injuries), and those over 70 (thereby excluding many infirm people, care home residents, etc.).
  • Therefore, this study provides no evidence that cranberry juice is effective in higher-risk women. Neither does the study look at the effects in men, or children and young people aged under 20. 
  • Cranberry juice is a very high-sugar drink that also contains a lot of additives. In fact, this study used a less additive-laden version with a shorter shelf life that is not commercially available. Therefore, people may need to individually consider whether the potential benefits of daily consumption of a high-sugar drink in the long term are worth it.
  • As the researchers acknowledge, effects may be different with consumption of cranberries in a different form, such as in powders or capsules, or the berry itself.

The researchers say their findings, "suggest that the consumption of cranberry is a useful strategy for reducing recurrent clinical UTI episodes and antibiotic use". However, the decision to try cranberry juice or not will need to remain an individual one.

It is estimated that half of all women will get a UTI at least once in their life, so the occasional infection is not usually a cause for concern. If you find yourself having repeated UTIs or persistent symptoms such as pain or irritation, or blood in your urine, then contact your GP. There may be underlying issues that need further investigation.

Links To The Headlines

Cranberry juice can reduce need for antibiotics by combating UTIs, research finds. The Daily Telegraph, June 20 2016

How cranberry juice can stave off infections: Compound in the fruit could reduce need for antibiotics because it prevents bacteria from sticking. Daily Mail, June 20 2016

Turns out cranberry juice might not do anything to help with UTIs. Metro, June 18 2016

Links To Science

Maki KC, Kaspar KL, Khoo C, et al. Consumption of a cranberry juice beverage lowered the number of clinical urinary tract infection episodes in women with a recent history of urinary tract infection. American Journal of Clinical Nutrition. Published online June 2016

Categories: NHS Choices

Could 5:2 diet play a role in preventing breast cancer?

Fri, 17/06/2016 - 13:45

"Women who follow the 5:2 diet 'could reduce their risk of breast cancer','' the Mail Online reports.

A small study found some women who followed the diet experienced breast cell changes thought to be protective against breast cancer. But the study was too small and too short to prove this is definitely the case.

The 5:2 diet is based on the idea that you eat a normal healthy diet for five days of the week and a fasting diet – recommendations are usually around 500 calories for women and 600 for men – for the other two days.

The study involved 24 women who were overweight or obese, aged 35 to 45, free of cancer or diabetes, and with a higher than average breast cancer risk.

The women were told to drop their calorie intake by 75% on two consecutive days a week and follow a Mediterranean diet for the remaining five.

The women lost weight and body fat – about 5% for both – and registered positive changes in the way their bodies were handling energy, fat and insulin.

Around half the women showed biochemical changes in their breast tissue that was interpreted as potentially related to breast cancer risk.

These changes fall a long way from proving that a 5:2 diet would reduce breast cancer risk in all women, although sustained weight loss is known to reduce breast cancer risk.

For more information, read the Behind the Headlines special report on the 5:2 diet.

Where did the story come from?

The study was led by researchers from the Genesis Breast Cancer Prevention Centre, University Hospital of South Manchester NHS Foundation Trust.

It was funded by Prevent Breast Cancer and Breast Cancer Now, both charities. The authors declared no conflicts of interest.

Published in the peer-reviewed Breast Cancer Research, the study is open-access, so it is free to view online and download.

The Mail Online covered the study facts accurately, but did not emphasise its many limitations – for example, the perils of generalising findings from around 20 women to all women with breast cancer. As such, its headline is potentially misleading.

What kind of research was this?

This small cohort study investigated the effects of an intermittent calorie-restricted diet on breast cancer risk.

Breast cancer is the most common type of cancer in the UK. But if it's treated early enough, it can be prevented from spreading to other parts of the body and the chances of survival are high.

Studies show that losing weight and restricting your energy intake are linked to lower breast cancer risk, but the specific effects of periodic or intermittent calorie restriction are not known.

This study wanted to test whether women on an intermittent diet would show any biochemical signs of a reduction in breast cancer risk.

A large study measuring calorie restriction over the long term, looking for links to diagnosed cases of breast cancer, would be a more reliable way of investigating this topic.

These sorts of studies can be time-consuming and expensive to run, though, so small studies like this also have their place and aim to make early inroads into the area.  

What did the research involve?

A small group of women followed a two-day-a-week calorie-restricted diet to see how it affected biological processes potentially related to breast cancer risk.

More than 800 women were invited to participate. Most ignored the invite and others were later excluded as ineligible, leaving a small select group of 24 who took part from start to finish.

The 24 recruits were obese or overweight women aged 35 to 45 with a higher than average risk of breast cancer (more than 17% lifetime risk) who were under surveillance by a Manchester genetic counselling clinic.

Only women who reported having low activity levels (less than 40 minutes of moderate activity a week), who had not had a breast scan in the last year, and who had a pre-specified breast density were allowed to take part. Women with conditions like diabetes or cancer were excluded.

The diet resembled a 5:2 diet, where calories are restricted on two consecutive days a week.

The researchers worked out how many calories each woman needed each day, and asked them to reduce them by 75% on two consecutive diet days a week over the period of one menstrual cycle – an average of 29 days in this group.

On calorie-restricted days the women had to get their 5 A DAY from 80g of vegetables and one 80g portion of fruit, as well as six portions of low-fat dairy produce, such as two pints of semi-skimmed milk.

For the other five days they followed a Mediterranean-style diet – 45% energy coming from low glycaemic index (GI) carbohydrates, 30% from fat, and 25% from protein. 

GI shows how quickly each food affects your blood sugar (glucose) level when carbohydrates are eaten.

A dietitian checked the women's compliance to the diet by reading food diaries they kept to log what they ate and drank.

Blood, urine, body fat and breast tissue samples were analysed before, during and at the end of the diet to monitor changes in body composition and breast cancer risk, including changes at a genetic level.

Four of the 24 women didn't have any genetic data available, so these findings relate to just 20 women.

Women were told to remain inactive, the logic being to keep physical activity constant so that any breast cancer risk changes might be attributed to changes in diet only. 

What were the basic results?

Women followed the diet with good compliance for an average of 29 days, achieving the 75% calorie reductions on two consecutive fast days as planned.

However, this influenced what happened on the next five days. There was a carryover effect whereby the women continued to reduce their calorie intake on five days, where it should have bounced back up to 100%.

They averaged 38% lower than this, meaning that over the seven-day week they were actually reducing their calories by around 45%, much more than the target.

Unsurprisingly, the women lost weight and body fat – averaging around 5% reductions in both. On the two low-calorie days, their bodies were much better able to deal with blood sugar efficiently. This continued on the other five days, although to a lesser extent.

The blood analyses showed 527 biochemical molecules significantly changed during the two calorie-restricted days – and the vast majority remained changed after five days of normal eating.

About half the women (11, 55%) showed signs of down-regulation to biochemical pathways involved in cell metabolism, making fats, and the way the body makes and metabolises energy sources.

Three women showed signs of changes to breast cancer-related genes involved in breast cell differentiation – the process a cell goes through to become specialised in a function or tissue – and collagen. Most women didn't have these changes.

How did the researchers interpret the results?

The authors' conclusions were unspectacular and accurate: "The transcriptional response to IER [intermittent energy restriction] is variable in breast tissue, which was not reflected in the systemic response, which occurred in all subjects."

They went on to say: "The mechanisms of breast responsiveness/non-responsiveness require further investigation." 


This study shows that intermittent calorie restriction has an immediate and fluctuating effect on our bodies that varies from person to person.

For the 24 inactive, overweight or obese, middle-aged women in this study, about half showed signs of genetic and biochemical changes to processes that might loosely be linked to breast cancer risk.

A very small number (three) had changes more directly associated with breast cells processes, but, again, loosely linked to breast cancer risk.

These links weren't consistent, clear or assessed over a long enough period to really know how the 5:2 diet or similar might affect breast cancer risk.

This means the study's findings don't support the Mail Online's headline that, "Women who follow the 5:2 diet 'could reduce their risk of breast cancer'."

Today's media coverage also implies that the tentative findings of between 3 and 11 women – those with the least vague chance of being linked to breast cancer – applied to most women with breast cancer.

If you pluck three people from a crowd of, say, 50,000 (the number of new invasive breast cancer cases each year in the UK in 2013) and try to make generalisations about specific parts of these people's lives, most people would clearly see you're more likely to get it wrong than right.

The same applies here. The study sample was small, and definitely not large enough to be able to make solid statements about breast cancer in general.

As the causes of breast cancer aren't fully understood, it's not known if it can be prevented altogether. 

Regular exercise and a healthy, balanced diet are recommended for all women because they can help prevent many conditions, including heart disease, diabetes and many forms of cancer.

Studies have looked at the link between breast cancer and diet, and although there are no definite conclusions, there are benefits for women who maintain a healthy weight, exercise regularly, and who have a low intake of saturated fat and alcohol.

Links To The Headlines

Women who follow the 5:2 diet 'could reduce their risk of breast cancer'. Mail Online, June 16 2016

Links To Science

Harvie MN, Sims AH, Pegington M, et al. Intermittent energy restriction induces changes in breast gene expression and systemic metabolism. Breast Cancer Research. Published online May 28 2016

Categories: NHS Choices

Coffee's cancer risk downgraded (as long as you don't drink it hot)

Thu, 16/06/2016 - 19:30

"Very hot drinks may cause cancer, but coffee does not, says WHO," The Guardian reports.

A review by the International Agency for Research on Cancer (IARC) concluded that only beverages consumed at higher than 65C posed a possible cancer risk.

The working group's report re-evaluated the cancer-causing properties of drinking coffee, maté (a South American drink), and very hot beverages.

Coffee was classified as a possible cause of cancer in 1991, but the group has cleared the previous classification and suggested any suspected link was because of the hot temperature of the drink.

The researchers concluded there was limited evidence that drinking coffee and maté causes cancer, but say the risk of cancer of the oesophagus – the gullet – may increase with the temperature of the drink above 65C (149F).

Both the Daily Mirror and Daily Mail covered the story. The Mirror reports that leaving your cup of tea for around five minutes should cool it to a safe level.

The Mail reports that, not entirely surprisingly, store-bought black coffee is hot, at between 66 and 81C. So again, it is best left to cool for a while.

As it stands, smoking or alcohol consumption pose a bigger – and better documented – risk for oesophageal cancer.

Read more about ways to reduce your cancer risk.

Who produced the report?

The report was published by an international collaboration of researchers (working group) of the IARC, a specialised cancer agency of the World Health Organization (WHO).

The group came together in France as part of the IARC Monographs Programme, which seeks to evaluate and identify environmental factors that can increase the risk of human cancer.

The researchers reviewed epidemiological studies of exposure to carcinogens in human populations, and used the evidence to classify potential hazards as:

  • group 1 – carcinogenic to humans
  • group 2A – probably carcinogenic
  • group 2B – possibly carcinogenic
  • group 3 – not classifiable (no evidence to make a reliable judgement)
  • group 4 – probably not carcinogenic

However, the classification does not indicate what level of risk is associated with the exposure to a classified hazard.

For example, smoking cigarettes and using a sunbed are both group 1 hazards. But the risk of cancer associated with smoking cigarettes is far higher than using a sunbed.

Overall, the exact method of how the authors identified and selected the research is unclear. As such, it's not possible to say that this was a systematic review.

The monographs are published so they can be used by national health agencies to support their actions in preventing exposure to potential carcinogens.

What did the report find?

As part of their re-evaluation, the group assessed more than 1,000 observational and experimental studies.

They concluded:

  • coffee drinking was "not classifiable as to its carcinogenicity to humans" (group 3)
  • maté was "not classifiable as to its carcinogenicity to humans" (group 3)
  • hot drinks above 65C were "probably carcinogenic to humans" (group 2A)

Coffee drinking was evaluated by the IARC in 1991, and at the time was classified as "possibly carcinogenic to humans" (group 2B).

However, this was based on "limited evidence" – defined on the basis that a positive association between hazard and outcome was observed, but bias could not be ruled out.

The current evaluation has been conducted on a much stronger and larger body of evidence, with nearly 500 relevant epidemiological studies identifying more than 20 different cancers.

The group assessed a collection of epidemiological evidence, and gave the greatest weight to prospective cohort and population-based case control studies that had controlled for other exposures, such as tobacco and alcohol consumption.

The studies followed cohorts of people who self-reported their coffee drinking habits to see how many individuals developed cancer and how it was related to their consumption of coffee.

During this re-evaluation, the majority of epidemiological studies showed no association between coffee drinking and cancers of the pancreas, female breast, and prostate. Reduced risks were observed for liver and endometrial cancers.

On judging the various studies, the group concluded the evidence for "coffee drinking causing cancer" was inadequate. Reasons included insufficient data, inconsistency of findings, inadequate control of potential confounders, and bias.


Maté is a hot drink consumed in South America, and is also the national drink of Argentina.

It's a caffeine-rich infusion made from dried leaves of the yerba maté plant. In 1991 the IARC classified it as "probably carcinogenic to humans" (group 2A).

Since then, several epidemiological studies have been conducted evaluating the risk of oesophageal cancer and the consumption of hot maté.

With this new data, the IARC wanted to better understand whether the associations from previous studies were the result of maté itself or the hot temperatures at which it is usually consumed.

The studies found cancer of the oesophagus was associated with drinking hot maté, rather than maté at warm or cold temperatures.

Hot drinks

The findings from the evaluations of maté led the researchers to assess the association between oesophageal cancer and other hot drinks.

Previous research from China, Iran, Japan and Turkey also found the risk of cancer may increase with the temperature of the drink.

The IARC conducted a combined analysis on several epidemiological studies that had assessed the effect of both temperature and the amount of maté consumed on 1,400 patients with oesophageal cancer.

The results showed that regardless of the amount consumed, the risk of cancer increased with an increase in temperature.

There were significant differences in the results from drinking very hot maté, but not with warm maté.

The studies suggested the carcinogenic effects occur when drinking at temperatures above 65C.

What are the implications?

The IARC monographs seek to identify potential cancer hazards to raise awareness that a certain exposure can cause cancer in exposed people. However, they don't issue recommendations.

Their assessment of scientific evidence is produced so the World Health Organization, health agencies and governments can take it into consideration when developing health policies and guidelines. Whatever actions are taken as a result remain in the hands of the authorities concerned.

Professor Tim Underwood, associate professor in surgery at the University of Southampton, said: "The bottom line here is that drinking very hot liquids is a cause of squamous cell cancer of the oesophagus, but the IARC classification can't tell us anything about the size of the risk – so we shouldn't take from this that there's a high risk of developing oesophageal cancer after drinking very hot drinks."

Professor Sir David Spiegelhalter, Winton professor of the public understanding of risk at the University of Cambridge, said: "Last year the IARC said that bacon is carcinogenic, but it became clear that when eaten in moderation it is not very risky.

"In the case of very hot drinks, the IARC conclude they are probably hazardous, but can't say how big the risk might be. This may be interesting science, but makes it difficult to construct a sensible response."

Arguably, a commonsense approach would be to not drink anything hot enough to give you a serious burn if you spilt it on yourself, whether it's maté, coffee or tea.

Links To The Headlines

Very hot drinks may cause cancer, but coffee does not, says WHO. The Guardian, June 15 2016

Cancer risk from coffee downgraded. BBC News, June 15 2016

Very hot drinks 'probably' cause cancer of the oesophagus, world health chiefs warn. Daily Mail, June 16 2016

Tea experts say cuppas do not cause cancer despite claims from health researchers. Daily Mirror, June 15 2016

Hot drinks probably cause cancer, warns World Health Organisation. The Daily Telegraph, June 15 2016

Links To Science

The International Agency for Research on Cancer Monograph Working Group. Carcinogenicity of drinking coffee, maté, and very hot beverages. The Lancet Oncology. Published online June 15 2016

Categories: NHS Choices

Brain scans find differences in 'badly behaved' teen boys

Thu, 16/06/2016 - 15:30

"'Striking' structural differences seen in study which compared brain scans of young men with antisocial behavioural problems with their healthy peers," The Guardian reports.

The results suggest these behavioural problems could have a neurological dimension.

Researchers used brain scanning techniques to compare the brain structure of groups of male children and adolescents with conduct disorder with matched healthy controls.

Conduct disorder is a type of personality disorder characterised by violent and disruptive behaviours that go way beyond typical naughty childish "acting up" or "teenage rebellion".

The study mapped the thickness of the brain's outer layer, comparing the thickness at different points, both within the groups and between the groups. They found boys who developed conduct disorder before the age of 10 had similarities in overlapping areas of outer brain thickness. This differed from boys without conduct disorder, and those who developed it in adolescence.

The study suggests that changes in brain development may contribute to conduct disorder, but it doesn't tell us the root cause of the condition. Crucially, we don't know what caused the differences in brain structure between the groups, or whether the same results would be found in larger samples.

An important point to bear in mind is that the structures of the brain have a high degree of plasticity, as they can change in response to external factors. So, hopefully, even if there is such a thing as a "conduct disorder" type of brain, this doesn't mean it cannot change.


Where did the story come from?

The study was carried out by researchers from the University of Southampton, University of Cambridge, University of Rome, Martinos Centre for Biomedical Imaging in Boston, Harvard Medical School, Gent University, Columbia University, the University of Bologna and the Medical Research Council.

It was funded by the Wellcome Trust, Medical Research Council, and Southampton and Cambridge Universities.

The study was published in the peer-reviewed Journal of Child Psychology and Psychiatry on an open-access basis, so you can read the paper for free online.

The best coverage was in The Guardian, which explained the techniques used, as well as the results and their limitations. The Daily Mail also gave a good overview.

The Daily Mirror and Daily Telegraph over-simplified the study, saying it had found certain areas in the brains of children with conduct disorder to be thicker, while the picture was more complex than that. The Mirror claimed researchers had "identified the roots of serious anti-social behaviour", which is not the case.

The Mirror's use of the term "delinquents" is also questionable and rather old-fashioned, conjuring up images of mods and rockers fighting on Brighton beach.


What kind of research was this?

This was a case control study, which used brain imaging (specifically MRI scans) to compare the brain structure of children and adolescents aged 13 to 21 with conduct disorder, with a group of the same age and sex (all male).

Case-control studies can show links between factors (such as brain structure and behaviour), but cannot show that one causes another.


What did the research involve?

Researchers recruited 95 boys and young men aged 13 to 21 from pupil referral units and youth offending services, who were interviewed and found to fit the diagnosis of conduct disorder. They also recruited 57 boys and young men of the same age from mainstream schools, without conduct disorder.

All the boys has MRI brain scans. Researchers analysed the scans to look for variations and similarities in the thickness of the outer layer of the brain – the cortex – within and between the groups.

The study was done in two phases, with separate scanners and different groups of participants at Cambridge and Southampton universities, to check that the results of the first phase could be repeated.

People who had been diagnosed with serious mental or physical illness, or with the developmental disorder autism, were not included in the study. As well as comparing brain scans between people with and without conduct disorder, the researchers looked at people who'd had child-onset conduct disorder (before the age of 10) and adult-onset (after age 10).

When carrying out the analysis, they adjusted their figures to take account of the following potential confounders:

  • age
  • IQ
  • overall brain size
  • whether the person also had attention deficit hyperactivity disorder (ADHD)


What were the basic results?

Boys and young men with conduct disorder dating from childhood had a distinct pattern of cortical thickness, showing variations in thickness in all four areas of the cortex, including the frontal, parietal, temporal and occipital cortices.

These patterns were not seen in boys and young men without conduct disorder, or with conduct disorder starting in adolescence. Those with adolescent-onset conduct disorder showed fewer correlations in cortical thickness, compared to those without conduct disorder.

The results held true after adjusting for confounding factors, and were similar in both the Cambridge and Southampton studies, which used different groups of participants.


How did the researchers interpret the results?

The researchers say their results suggest that both child- and adolescent-onset conduct disorder "are associated with changes in the synchronised development of the brain". They say this shows that "neurobiological factors" are important contributors to the development of conduct disorder, whether in childhood or adolescence. They suggest that brain scans might be of use in testing treatments for conduct disorder in the future.

They say their findings are "among the first" to show "marked differences in brain structure" between the child-onset and adolescent-onset forms of conduct disorder, and that this suggests the age at which the disorder begins is important.

They warn that "the biological underpinnings of interregional correlations in cortical thickness are not well understood," so any suggestions about why the brain develops differently in people with conduct disorder are speculative.



This interesting study raises a lot of questions about the way the brain develops in childhood and adolescence, and whether its development is different in those with conduct disorder. However, it doesn't give us answers as to why this might happen.

The results suggest there are differences in the development of these children's brains, which may play a part in their condition. However, as with all observational studies, we can't tell from the study whether these brain differences are the cause of the conduct disorder.

The study also showed that substance abuse and deprivation were more common among boys with child-onset conduct disorder, suggesting they might also play a part.

The study only looked at boys, so we don't know whether the findings would apply to girls with conduct disorder. It's important to be aware that the results only showed areas of overlap between cortical thickness at certain areas of the brain in boys with this disorder, not a defined "map" of brain structure in this condition, so (for example) brain scans could not be used at this stage to diagnose conduct disorder.

Conduct disorder is a challenging condition for parents and schools to manage. Until the causes are better understood, it will be difficult to find useful treatments. Studies such as these are a starting point for finding out more about what causes conduct disorder.  

Links To The Headlines

First brain map of teenage delinquents 'shows they're wired differently to children who behave'. Daily Mirror, June 16 2016

Unruly pupils may have brain abnormalities, study suggests. The Telegraph, June 16 2016

Scans show differences in brains of problematic teenage boys. Daily Mail, June 16 2016

Scans show possible link between brain development and antisocial behaviour. The Guardian, June 16 2016

Categories: NHS Choices

Three servings of wholegrains a day 'cuts risk of early death'

Wed, 15/06/2016 - 17:40

"Eating Weetabix for breakfast 'can slash your risk of dying early from any cause'," the Daily Mirror reports.

A new study looking at wholegrain consumption (not just Weetabix) found a strong link between consumption and improved "long-term health and longevity" compared with people who ate little or no wholegrain.

This study pooled data from 14 large studies, which included 786,076 people. It found that the chances of dying from any cause during study follow-up was 16% lower for people who ate the most wholegrain, compared to those who ate the least. The link was strongest when the researchers looked at deaths from heart attacks and strokes. There was a weaker link to a lower risk of dying from cancer.

We can't be sure that all the reduced risk is solely down to eating wholegrain food, as people who eat wholegrain may also have other patterns of healthy behaviour, such as exercising regularly and avoiding smoking and excessive alcohol consumption.

While some of the studies attempted to account for these types of factors (confounders), it is challenging to filter these influences from analysis.

Nevertheless, this study adds to the evidence that wholegrain foods are an important part of a healthy diet, and should be picked in preference to refined carbohydrates (such as white bread, rice and pasta). Current advice is that healthy starchy food options should make up just over a third of the food we eat. 

Where did the story come from?

The study was carried out by researchers from Harvard TH Chan School of Public Health and Harvard Medical School, and was funded by the National Institutes of Health in the US. The study was published in the peer-reviewed medical journal Circulation.

The Mirror's odd fixation on Weetabix could lead readers to conclude that the study looked only at that brand of breakfast cereal, instead of all types of wholegrain food, including bread, rice, pasta and other types of muesli or cereal. All we can guess is that the photo desk had an image of Weetabix to hand.

The Daily Mail gave a better overview of the study, although the claim that "three slices of wholemeal bread a day slash the risk of dying of heart disease by 25%" is slightly exaggerated. The actual risk reduction for eating 70g a day of wholegrain food, compared to eating no wholegrain food, was 23%.


What kind of research was this?

This was a systematic review that pooled the findings of prospective cohort studies in a meta-analysis to try to better establish whether eating wholegrains is linked with mortality risk.

A meta-analysis is a good way of summarising the results of all studies in a specific area. Prospective cohort studies can help identify links between an exposure and an outcome – in this case, wholegrain food and mortality. But cohort studies can't show whether one factor causes another, usually because other health and lifestyle factors may be involved in the link.


What did the research involve?

Researchers searched literature databases to identify all prospective cohort studies looking at wholegrain intake and mortality. They excluded any studies where it was not possible to estimate wholegrain intake.

They pooled the results, looking separately at death from any cause, death from cardiovascular disease (CVD) and death from cancer.

As well as cohort studies looking specifically at wholegrain, the researchers included data from large surveys of diet and health in the US, known as the National Health and Nutrition Survey (NHANES) which allowed them to include a much bigger data set.

Researchers used the data to calculate the "dose response" to wholegrain, looking at the effect of eating 10g, 50g and 70g of wholegrain a day. One serving (i.e. one slice of bread or bowl of cereal) contains roughly 16g.

Overall, 14 studies met eligibility criteria, most of which (10) were carried out in the US. The studies were conducted between 1971 and 2010 and had follow-up periods ranging from 6 to 28 years.


What were the basic results?

There were 97,867 deaths recorded among the 786,076 people who took part in the studies (so 12.5% of people died).

People who ate the most wholegrain food had a 16% lower chance of dying during the studies, compared to people who ate the least wholegrain food (relative risk [RR] 0.84, 95% confidence interval [CI] 0.8 to 0.88), and had a 18% lower chance of dying from cardiovascular disease (RR 0.82, 95% CI 0.79 to 0.85). They also had a 12% reduced risk of dying from cancer (RR 0.88, 95% CI, 0.83 to 0.94).

An additional serving of wholegrain food each day reduced the risk of dying from any cause by about 7% (RR 0.93, 95% CI 0.92 to 0.94). The researchers calculated that if everyone in these studies had been eating high amounts of wholegrains, this would have reduced the observed mortality rate by about 10%, with similar reductions for cardiovascular and cancer deaths specifically.


How did the researchers interpret the results?

Researchers said the study showed that eating wholegrain food "was inversely associated with mortality in a dose-response manner". In other words, it reduced the chances of death depending on the amount eaten, and that "the association with CVD mortality was particularly strong and robust".

They say this reinforces the current dietary guidelines to eat at least three servings of wholegrain food a day, and to replace refined carbohydrates with wholegrains.



This large, carefully conducted review adds to the evidence we already have that wholegrain food is a healthy part of a balanced diet, and that eating less refined carbohydrates (such as white bread) and more wholegrain alternatives is a good move.

Due to the observational nature of these studies, we cannot be sure that the entirety of the reduced risk of early death is due to eating wholegrains. People who choose wholegrain food may be more likely to live a healthy lifestyle in other ways – for example, they may be less likely to smoke or drink alcohol to excess, and be more likely to exercise.

While the cohort studies adjusted their figures to take account of many confounding factors, we can't be sure they accounted for all of them. The number of confounding factors that each of the studies accounted for varied, but they all took account of smoking.

Most of the studies were carried out in the US, with one from the UK and three from Scandinavia. This means the results may not be applicable to populations with different diets and ethnic backgrounds.

The studies were also conducted over different eras – for example, some looked at the 1970s to 1980s, and others looked at the 00s to 10s. Food availability, dietary patterns and lifestyle may not be directly comparable across different studies. There is also the possibility with all food frequency assessments to inaccurately recall the type and quantity of particular food groups.

Therefore, though the review can't prove that wholegrains were solely responsible for the mortality reduction seen, the evidence that wholegrain food is good for health remains strong, especially for cardiovascular health.

Links To The Headlines

Eating Weetabix for breakfast 'can slash your risk of dying early from any cause'. Daily Mirror, June 13 2016

Three slices of wholemeal bread a day slash risk of dying from heart disease by 25%. Daily Mail, June 13 2016

Links To Science

Zong G, Gao A, Ju FB, Sun Q. Whole Grain Intake and Mortality From All Causes, Cardiovascular Disease, and Cancer - A Meta-Analysis of Prospective Cohort Studies. Circulation. Published online June 13 2016

Categories: NHS Choices

Teens who vape e-cigs 'six times more likely to smoke cigarettes'

Tue, 14/06/2016 - 13:30

"Vaping is a gateway to smoking," the Mail Online reports, seriously overstating the evidence of a new US study.

While the study did find teens who experimented with e-cigs were more likely to smoke "traditional" tobacco products – mainly cigarettes – no direct link between the two was proven.

Following a survey, around 300 adolescents aged 17 from California who had never smoked tobacco were included in the study. Half of them had used e-cigarettes.

Sixteen months later, those that had smoked e-cigarettes were six times more likely to have started smoking tobacco.  

An obvious response to this finding is that certain teenagers are less risk-averse than others – those who experimented with e-cigarettes would have probably ended up trying cigarettes anyway, regardless of whether or not e-cigarettes existed.

The researchers did try to account for this effect by asking teenagers at the beginning of the study if they had a "firm commitment" to never start smoking. But you could make the case that nothing changes faster than a teenager's mind.

So, in spite of the Mail's headline, this study is not able to prove the use of e-cigarettes is responsible for a progression to smoking.

Rates of teen smoking are low in England, at around 4% for under-16s. The increasing popularity of e-cigarettes has not had any impact on this welcome trend – at least at the moment.

Under recent legislation, it is now illegal to supply e-cigarettes to under-18s, unless they have a prescription.

Where did the story come from?

The study was carried out by researchers from the University of Southern California.

It was funded by the US National Cancer Institute at the National Institutes of Health and the Food and Drug Administration Center for Tobacco Products.

The study was published on an open access basis in the peer-reviewed journal Pediatrics, so it is free to view online.

While the Mail reports the study accurately in the body of its report, its headline "Vaping is a gateway to smoking" is unsupported by the evidence from the study.

What kind of research was this?

This prospective cohort study aimed to assess whether the use of e-cigarettes in adolescents leads to the use of combustible tobacco products such as cigarettes, cigars and pipes.

This type of study is able to make a link between vaping and smoking, but it is unable to prove e-cigarettes are the cause of adolescents progressing to smoking.

What did the research involve?

The researchers included adolescents in the eleventh and twelfth grade from high schools in south California, with an average age of 17.

At the start of the study, teenagers filled out a questionnaire under the supervision of research staff, designed to evaluate whether they had smoked tobacco or used e-cigarettes.

They were asked whether they had tried e-cigarettes, cigarettes, cigars, pipes or hookah in the past 30 days, classified as "never tried" and "ever users".

The researchers restricted their analyses to those who had never smoked cigarettes at the first evaluation.

Susceptibility to cigarette use was defined as the "absence of a firm commitment not to smoke".

When questioned about intention to smoke in the future, students who answered "definitely not" were considered "not susceptible".

The researchers also asked questions about the social acceptability of smoking within the teenagers' social environment.

Questions and possible responses were as follows:

  • How many of your four closest friends use cigarettes? (0 to 4 friends)
  • How would your best friends act toward you if you used cigarettes? (very unfriendly, unfriendly, friendly, or very friendly)
  • Does anyone who lives with you now use cigarettes? (yes or no)

Information on sociodemographic factors was also collected.

The researchers then invited the never-smoking e-cigarette users and a sample of never-smoking and never e-cigarette users to complete a follow-up questionnaire 16 months later.

Never-users were matched to e-cigarette users by gender, ethnicity and grade.

What were the basic results?

The study presented findings from 152 never users and 146 e-cigarette users.

Cigarette smoking during the follow-up period was reported by 40.4% of e-cigarette users and 10.5% of those who had never vaped.

After adjusting for possible confounders, e-cigarette users were 6.17 times more likely to start smoking cigarettes than never e-cigarette users (95% confidence interval 3.30 to 11.6).

E-cigarette users were more likely to start using any combustible product, including hookah, cigars and pipes.

How did the researchers interpret the results?

The researchers concluded: "E-cigarette use in never-smoking youth may increase risk of subsequent initiation of cigarettes and other combustible products during the transition to adulthood, when the purchase of tobacco products becomes legal.

"Stronger associations in participants with no intention of smoking suggests that e-cigarette use was not simply a marker for individuals who would have gone on to smoke, regardless of e-cigarette use." 


This prospective cohort study found adolescents who used e-cigarettes were more likely to go on to use combustible tobacco products such as cigarettes, cigars and pipes than those who never used e-cigarettes.

But the strength of these findings is limited by a number of factors:

  • The study design is not able to prove the use of e-cigarettes is responsible for progression to smoking. However, the researchers did attempt to investigate susceptibility in both e-cigarette users and non-users.
  • The sample of participants was small, from a particular age group and from one location, reducing the reliability and generalisability of the findings.  
  • No information was collected on the type of e-cigarette used or nicotine content.
  • A large number of participants were lost to follow-up – whether these teens went on to smoke or not would have altered the results.
  • The initial grouping of participants into users and non-users was based on their responses to a questionnaire completed with a researcher. Students may have felt the need to give responses they felt were more appropriate, rather than accurate.

Under new legislation, it is now illegal to sell e-cigarettes – and e-liquids, or nicotine-containing liquid – to under-18s, unless they have a prescription for a brand of e-cigarette recognised as a stop-smoking aid.

Read more advice about helping teens quit smoking.

Links To The Headlines

Vaping is a gateway to smoking: Teenagers who use e-cigarettes 'are six times more likely to smoke tobacco'. Mail Online, June 13 2016

Links To Science

Barrington-Trimis JL, Urman R, Bernhane K, et al. E-Cigarettes and Future Cigarette Use. Pediatrics. Published online June 13 2016

Categories: NHS Choices

Study says there's no link between cholesterol and heart disease

Mon, 13/06/2016 - 15:40

"Controversial report claims there's no link between 'bad cholesterol' and heart disease," the Daily Mail reports, while The Times states: "Bad cholesterol 'helps you live longer',".

The headlines are based on a new review which aimed to gather evidence from previous observational studies on whether LDL cholesterol (so-called "bad cholesterol") was linked with mortality in older adults aged over 60. The conventional view is that having high LDL cholesterol levels increases your risk of dying of cardiovascular diseases, such as heart disease.

Researchers chose 30 studies in total to analyse. 28 studies looked at the link with death from any cause. Twelve found no link between LDL and mortality, but 16 actually found that lower LDL was linked with higher mortality risk – the opposite to what was expected.

Only nine studies looked at cardiovascular mortality link specifically – seven found no link and two found the opposite link to what was expected.

However, there are many important limitations to this review. This includes the possibility that the search methods may have missed relevant studies, not looking at levels of other blood fats (e.g. total and HDL cholesterol), and the possibility that other health and lifestyle factors are influencing the link.

Most importantly, as the researchers acknowledge, these findings do not take account of statin use, which lowers cholesterol. People found to have high LDL cholesterol at the study's start may have subsequently been started on statins, which could have prevented deaths.  

Where did the story come from?

The study was carried out by researchers from the University of South Florida, the Japan Institute of Pharmacovigilance and various other international institutions in Japan, Sweden, UK, Ireland, US and Italy.

Funding was provided by the Western Vascular Institute. The study was published in the peer-reviewed BMJ Open and, as the journal name suggests, the article is open-access, so can be read for free.

Four of the study authors have previously written book(s) criticising "the cholesterol hypothesis". It should also be noted that nine of the authors are members of THINCS – The International Network of Cholesterol Skeptics. This is described as a group of scientists who "oppose…that animal fat and high cholesterol play a role [in heart disease]".

If you were playing Devil's Advocate, you could argue that this represents a preconceived view of the authors regarding the role of cholesterol, rather than the open, unbiased mind you would hope for in the spirit of scientific enquiry. That said, many important scientific breakthroughs happened due to the efforts of individuals who challenged a prevailing orthodoxy of thinking.

In general, the UK media provided fairly balanced reporting, presenting both sides of the argument – supporting the findings, but with critical views from other experts.


What kind of research was this?

This was a systematic review which aimed to gather evidence from cohort studies to see whether LDL – "bad" – cholesterol is associated with mortality in older adults.

It has long been thought that cholesterol is a key cause of the fatty build-up in arteries (atherosclerosis) that causes heart disease. However, the researchers say there are contradictions to this view. Recent research has suggested that total cholesterol becomes less of a risk factor for all-cause or cardiovascular mortality the older people get. Less is known about LDL specifically and that's what this research aimed to look at.

A systematic review is the best way of gathering evidence from cohort studies that have looked at the link between an exposure or risk factor and an outcome. However, the strength of a review's findings is only as good as the studies they include. In cohort studies, it is often difficult to directly attribute an outcome to a specific cause, and there is always the potential that other factors are influencing the outcome. 


What did the research involve?

The researchers searched one literature database (PubMed) in December 2015 to identify English-language cohort studies that had included a general population sample aged 60 and over. Studies had to have taken baseline measures of LDL cholesterol and then followed participants up over time, looking at the link with all-cause or cardiovascular mortality.

Three authors reviewed potential studies and extracted data. From an initial 2,894 hits, 19 publications, covering 30 cohorts and including 68,094 participants, were included. The majority of studies were excluded outright, as they didn't seem to contain anything relevant in the study title or abstract (summary). The other reasons for exclusion were non-English language, participants not being representative of the general population, not measuring LDL cholesterol at baseline, and not giving separate data for older adults or looking at mortality outcomes.


What were the basic results?

The researchers did not pool the results of the individual cohorts in a meta-analysis, but gave a narrative summary of the findings.

Overall, they reported that 16 cohorts (representing 92% of individuals in the review) of 28 examining all-cause mortality found an inverse relationship between LDL cholesterol and all-cause mortality. That is, as LDL cholesterol went down, all-cause mortality went up – higher LDL was apparently linked to lower all-cause mortality. In 14 of these 16, this was said to be a statistically significant link. The remaining 12 cohorts found no link with all-cause mortality.

Only nine of the identified cohorts specifically reported cardiovascular mortality. Seven found no link between LDL cholesterol and cardiovascular mortality. The other two found that those in the lowest fourth (quartile) of LDL levels actually had the highest cardiovascular mortality.


How did the researchers interpret the results?

The researchers concluded that, "High LDL-C is inversely associated with mortality in most people over 60 years". They said their finding contradicts the cholesterol hypothesis: that cholesterol, particularly LDL, causes fatty build-up in the arteries. 

They consider that as they found older adults with high LDL live just as long as those with low LDL, this "provides the rationale for a re-evaluation of guidelines recommending pharmacological reduction of LDL-C in the elderly".



This research suggests that – contrary to common belief – LDL cholesterol is not as "bad" as may be thought, and higher levels are not linked to all-cause or cardiovascular mortality.

However, before accepting this as fact, there are many important limitations to consider – both to the review and the included studies – many of which the review authors themselves acknowledge:

  • There is the potential that many studies relevant to this question may have been missed out. The review searched only a single literature database, excluded studies only available in non-English language, and excluded studies where the title and abstract did not appear to contain information on the link between LDL and mortality in older adults.
  • The study only looked at the link in older adults aged over 60. LDL-cholesterol levels may show different links with long-term mortality in younger adults. Though this was intended to represent the general older-age population, some studies had excluded people with specific conditions such as dementia, diabetes or terminal illness.
  • The studies varied widely in adjustment for confounding factors that could be having an influence on the link between LDL and mortality. Age, gender and body mass index (BMI) were common factors that studies took into account, but others variably accounted for lifestyle factors (e.g. smoking, alcohol), socioeconomic factors, presence of conditions, and use of medications.
  • Only LDL cholesterol was examined. Levels of total cholesterol, trigylcerides, and the ratio of LDL to HDL "good" cholesterol could be having an effect and mediating the link between LDL and mortality.
  • Most of the evidence for this review is for the link with all-cause mortality – not cardiovascular mortality. High LDL-cholesterol is believed to be linked with the development of atherosclerosis and cardiovascular disease. This review does not provide enough firm evidence to refute this link. The review cannot with certainty explain the reasons for the apparent link between LDL levels and death from any cause – with roughly half of studies finding a link and half not.
  • Importantly, the study does not provide evidence that statins are "a waste of time". These are not trials examining mortality between people prescribed statins or not. The researchers openly acknowledge that the use of statins – which they haven't directly examined – may be confounding the links in these studies. For example, the people found to have the highest LDL cholesterol levels at the study's start may have then been started on statins, and this could have dramatically cut their reduced mortality risk.

The findings of this review and possible explanations will need to be explored further, but for now this review doesn't provide solid evidence that high LDL cholesterol is good for you, or that statins are of no help. People given statins should continue to take them as prescribed.

"Fat is actually good for you" may be a great headline for a newspaper, and there are always researchers who are willing to make such a case, as we saw with the recent National Obesity Forum report.

These types of stories are often based on a selective view of evidence, rather than a comprehensive systematic review. There is currently no comprehensive body of evidence that contradicts current official advice on saturated fat consumption – which recommends no more than 30g of saturated fat a day for men and 20g for women.

Links To The Headlines

Statins 'may be a waste of time': Controversial report claims there's NO link between 'bad cholesterol' and heart disease. Daily Mail, June 13 2016

High cholesterol 'does not cause heart disease' new research finds, so treating with statins a 'waste of time'. The Daily Telegraph, June 13 2016

Health experts slam study that suggests over-60s live longer with 'bad cholesterol'. Daily Mirror, June 12 2016

Bad cholesterol ‘helps you live longer’. The Times, June 13 2016 (subscription required)

Don't throw away your statins yet - LDL cholesterol is probably still bad for you. The Guardian, June 13 2016

Links To Science

Ravnskov U, Diamond DM, Hama R, et al. Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review. BMJ Open. Published online June 12 2016

Categories: NHS Choices

Risky stem cell treatment 'halts progress of multiple sclerosis'

Fri, 10/06/2016 - 14:30

"New treatment can 'halt' multiple sclerosis, says study," BBC News reports.

The treatment involves effectively destroying the existing immune system and creating a new one using stem cells. But this new treatment carries a high risk of complications.

Multiple sclerosis (MS) is a life-long condition that affects the brain and spinal cord, causing a wide range of symptoms, including problems with arm or leg movement, vision, sensation and balance, and serious disability.

It is an autoimmune disease where the immune system mistakenly attacks healthy cells in the body – in this case, the coating of the nerves (myelin sheath).

In this Canadian study, researchers essentiality destroyed a patient's existing immune system with a very aggressive course of chemotherapy drugs.

They then transplanted stem cells – which have the potential to become any type of blood cell – in an attempt to rebuild an immune system without the flaws that trigger MS.

Of the 24 patients that took part in the study, 70% had no disease activity three years after the transplant, and about a third had sustained improvement in disability status. For example, 16 patients were able to go back to work or college.

One fact to bear in mind, however, is that this was a small study with no comparison group, and one of the 24 patients died after transplant as the result of an infection.

This represents a mortality rate of 4%. Whether or not this was just an unfortunate one-off is unclear.

The risks and benefits of this approach need to be carefully weighed and compared before it can be widely adopted in clinical practice.

Where did the story come from?

The study was carried out by researchers mostly from medical institutions in Canada, as well as three researchers from the Department of Neurosciences, Cleveland, in the US.

It was funded by grants from the Multiple Sclerosis Scientific Research Foundation. Some of the researchers also received personal fees and grants from a number of pharmaceutical and biotech companies.

The study was published in the peer-reviewed journal, The Lancet.

While the UK media was along the right lines reporting news of a 'breakthrough treatment', it is slightly premature considering this is a very small, early stage, study.

The media did, however, go on to highlight that further investigation was needed before this treatment becomes available in clinical practice.

It was also correctly reported that this treatment wouldn't be suitable for many people with less debilitating MS because of the risks it carries.

What kind of research was this?

This phase II trial aimed to assess a new treatment approach of aggressive chemotherapy followed by haemopoietic stem cell transplant (HSCT).

The researchers wanted to see whether this had an impact on clinical relapse and improvements in disability in people with multiple sclerosis.

Haemopoietic stem cells are very early-stage blood cells that can develop into all other types of blood and immune cells.

This study involved autologous HSCT, where stem cells are first harvested from the patient before high-dose chemotherapy is given to deplete the person's own cells.

The harvested cells were then transplanted in the hope this would allow the immune system to be rebuilt without the flaws that trigger MS.

This is an early-stage clinical trial involving a relatively small number of people and no comparison group. It aimed to see whether the treatment is safe and could potentially be effective.

This is important early-stage research designed to see whether the findings are promising, and may pave the way for further investigation in later trials involving more people and comparisons with other treatments or placebo. 

What did the research involve?

The study began in the year 2000, when researchers recruited 24 patients between the ages of 18 and 50 from three hospitals in Canada.

Their disease was defined as having a high probability of significant progression over the next 10 years, having suffered multiple relapses prior to being enrolled in the study.

The patients first had their haemopoietic stem cells harvested, and their immune system was then fully suppressed with aggressive chemotherapy. They then received HSCT two days after their final dose of chemotherapy. 

The main outcome of interest was the proportion of patients who were surviving and free from MS disease activity three years after transplant.

This was assessed by looking at clinical relapse, appearance of new MS lesions on MRI scans, and sustained improvements in disability status.

Of the 24 patients, 21 were followed up to three years, and 13 took part in longer-term follow-up. The average follow-up duration was 6.7 years (range 3.9-12.7).

What were the basic results?

Overall, 17 of the 24 patients (69.9%) achieved activity-free survival three years after transplantation. The remaining seven patients had sustained progression of disability.

Clinical relapses did not occur in any of the 23 surviving patients during follow-up. These results were mirrored by no new lesions being seen on 314 sequential MRI scans overall. And 35% of patients had sustained improvements in their disability status.

One patient died of transplantation-related complications, however. There were also various side effects associated with treatment.

Most patients experienced toxicity effects of varying degrees of severity, and fever and infections were common.

How did the researchers interpret the results?

The researchers concluded: "We describe the first treatment to fully halt all detectable CNS [central nervous system] inflammatory activity in patients with multiple sclerosis for a prolonged period in the absence of any ongoing disease-modifying drugs.

"Furthermore, many of the patients had substantial recovery of neurological function despite their disease's aggressive nature." 


This early-stage trial aimed to look at a new treatment approach for MS, involving aggressive chemotherapy followed by haematopoietic stem cell transplant (HSCT). Researchers then assessed whether this had an impact on clinical relapse and disability.

The study suggests that eliminating an individual's existing "faulty" immune system, and rebuilding it using stem cells, may slow down or completely halt the progression of MS, resulting in an improvement in disability status.

Although the study's findings suggest this could be a potential treatment in the future, the researchers say caution is necessary before it is widely adopted in clinical practice.

This was very early-stage research, with a small sample size and no control group for comparison with those who were treated.

The findings were positive overall, but the retention to longer-term follow-up was quite low, with only around half being followed up beyond three years.

This means although there were no documented relapses and around a third improved functional ability during follow-up, these results could be different with a much larger sample size.

Also, the fact there was one death among the 24 treated patients and toxic side effects were common cannot go unnoticed.

Dr Payam Rezaie, a reader in neuropathology at The Open University, commented: "While this study does add considerable weight to the use of autologous HSCT as a therapeutic approach for MS, it is difficult to make a more generalised inference on its use, based on this study alone.

"The risks need to be carefully weighed when compared with the beneficial outcomes. The present study indicates a need to examine this further."

Further trials in larger groups of people with MS, including those with different disease characteristics, and comparing it with other treatments, would be needed to better gauge the effectiveness and safety of this approach.  

Links To The Headlines

New treatment can 'halt' multiple sclerosis, says study. BBC News, June 10 2016

Stem cell therapy gives hope to MS patients. The Guardian, June 9 2016

Breakthrough treatment for multiple sclerosis found to reverse symptoms. The Independent, June 10 2016

Hope for multiple sclerosis cure as 23 seriously ill patients recover after 'breakthrough' stem cell treatment. The Daily Telegraph, June 10 2016

Stem cell treatment 'can halt symptoms of multiple sclerosis', scientists discover. Daily Mirror, June 9 2016

Radical treatment can halt and even reverse progress of multiple sclerosis. The Sun, June 10 2016

Links To Science

Atkins HK, Bowman M, Allan D, et al. Immunoablation and autologous haemopoietic stem-cell transplantation for aggressive multiple sclerosis: a multicentre single-group phase 2 trial. The Lancet. Published online June 9 2016

Categories: NHS Choices

Should we rethink the causes of anorexia?

Thu, 09/06/2016 - 16:30

"Anorexia is not about a fear of getting fat, but rather a pleasure at losing weight, experts reveal," says the Daily Mail. The headline oversimplifies the results of a study that looked at women's responses to photos of women of varying weights.

In the study, 71 women with anorexia and 20 without were shown photographs of women who were either a normal weight, underweight or overweight, while monitors recorded sweating caused by emotional excitement. This type of test, known as a skin conductivity test, is reported to be a way of assessing levels of emotional excitement.

Researchers found women with anorexia felt more negatively about images of normal and overweight women, and more positively about images of underweight women, compared with women without anorexia.

This suggests a desire to be thin may be more important than a fear of getting fat, say the researchers. This hypothesis, unproven as it currently is, could explain the continuing popularity of "pro-ana" websites. These sites often use pictures of underweight women to promote the so-called "anorexia lifestyle".

The researchers also tried to see if this "getting thin is pleasurable" attitude was linked to a specific gene type known as Val66Met, but the results were inconclusive.

Anorexia carries the highest risk of death among all mental health conditions. If you are worried you may have anorexia or someone you know has it, it's important to get medical help as soon as possible. You can start with your GP, or by visiting the Beat, a UK charity supporting people with eating disorders.

Where did the story come from?

The study was carried out by researchers from Paris-Descartes University and INSERM UMR in France, and the University of Ulm in Germany.

It was funded by Fonds d'Etudes et de Recherche du Corps Médical.

The study was published in the peer-reviewed journal Translational Psychiatry on an open-access basis, so you can read it for free online.

Despite the Mail's over-simplifying headline, its report covers the study well. Unfortunately, the article is illustrated by a photograph of a very thin young woman in her underwear, exactly the sort of image the study suggests may motivate women with anorexia.


What kind of research was this?

In this case control study, researchers compared the reactions of 20 healthy women with the reactions of 71 women with anorexia when they were shown images of underweight, normal weight and overweight women.

Researchers wanted to know which images provoked the strongest responses in women with anorexia, and whether that was different from healthy women.

Studies like these can help us understand more about an illness, but they can't prove causality – so, in this case, we don't know if the women's reactions are a cause of anorexia, or perhaps a symptom of the disorder, or if they're related in some other way.


What did the research involve?

Researchers recruited 71 women being treated for anorexia at a hospital in Paris, and 20 of their friends or acquaintances of a similar age and education level.

The women were shown 120 images over four sessions, while answering questions about them and having their skin response monitored. Afterwards, researchers compared the results between women with and without anorexia.

The women with anorexia had a mixture of conditions (food restriction or binge/purge) and were at a range of weights. Some were no longer clinically underweight, having put on weight since starting treatment. Half of them were treated as in-patients.

All women were asked to categorise the images they were shown by estimated weight, and to say how they would feel on a scale of one to four if that was their body (one being very unhappy, four being very happy).

They wore devices on their hands that tested skin conductivity to measure the rate of sweating caused by emotional excitement as they watched the images.

This measure was included as a truer measure of reaction, as some women may have felt they were supposed to react in certain ways to images of people who were over- or underweight.

All women also had their saliva analysed for a type of gene (Val66Met) that has been linked to anorexia, although the link is unproven.

Researchers analysed the data for a range of groups and sub-groups. They looked at whether women with anorexia reacted differently from women without, and whether women's weight or length of illness affected the results.

They also looked at how many women carried the gene associated with anorexia, and whether that affected the results.


What were the basic results?

Women with anorexia were more likely to overestimate the weight of people in the images who were underweight and normal weight.

Women with anorexia were likely to be less happy with the thought of having a body like the normal-weight images (average score 1.9, compared with 2.6 for healthy women) and slightly less happy than healthy women at the thought of having a body like the overweight image.

They were happier with the thought of having a body like the underweight images (average score 2.7, compared with 1.9 for healthy women).

Results of skin conductivity tests found women with anorexia were more likely to show a response to underweight images than healthy women were. They were also more likely to show a response to underweight images than overweight or normal weight images.

Carriers of the gene type linked to anorexia were more likely to show a skin conductivity response to images of underweight women, compared with those without this gene type.


How did the researchers interpret the results?

The researchers say their results "suggest an increased attention and motivation toward underweight stimuli [i.e. images of underweight women]" among women with anorexia, which "may promote pathological behaviours, maintaining starvation in patients".

In other words, they believe that viewing images of underweight bodies might encourage people with anorexia to persist in eating too little.

The researchers say their results showed the positive feelings towards images of underweight bodies were stronger than negative feelings towards overweight bodies.

They say having a "positive value of starvation, rather than a more negative value of overweight" might be a more accurate definition of anorexia than the current definition, which emphasises an intense fear of weight gain. They add that the gene type investigated "could partly mediate" this response.



Anorexia is a notoriously difficult illness to treat. While people do recover, many live with this devastating condition for years, and some die from it.

Because anorexia is so difficult to cure, researchers are interested in finding out more about how the condition works. A better understanding of the underlying causes might help find better treatments.

This study is an interesting addition to that understanding. A primary feature of anorexia was always thought to be fear of weight gain, and many people with anorexia say they do fear putting on weight.

But this study found that a desire to be very thin may be as important, or possibly more important, than a fear of gaining weight.

There are some important caveats. Showing an electrical reaction in the skin when people look at images of underweight bodies, and hearing that people with anorexia would be happy to have an underweight body, is not the same as proving that a desire to be thin underlies the illness.

The electrical reaction was assumed to be one of excitement, but it could equally have been one of increased anxiety.

The study involved only 71 people, with different types of anorexia and at different stages in their illness. A bigger study with more specific groups might help us understand more.

For example, we don't know whether a preference for underweight body types triggers anorexia, or whether this preference is learned as anorexia develops.

The control group only included 20 people, meaning their results might not be representative of all healthy women. This would change the effect of comparing responses from women with anorexia to responses from healthy women.

The findings relating to the gene type are quite tenuous. For one thing, the gene type was as common among women without anorexia as with it. More work needs to be done to understand whether genetics does have a role to play in the condition.

Links To The Headlines

Anorexia is not about a fear of getting fat, but rather a pleasure at losing weight, experts reveal. Daily Mail, June 9 2016

Links To Science

Clarke J, Ramoz N, Fladung AK, Gorwood P. Higher reward value of starvation imagery in anorexia nervosa and association with the Val66Met BDNF polymorphism. Translational Psychiatry. Published online June 7 2016

Categories: NHS Choices

Green tea extract 'boosts mental ability' in people with Down's

Wed, 08/06/2016 - 13:00

"Down's syndrome can be treated with green tea," says The Daily Telegraph, reporting on a study that looked at the effect of a chemical extract on learning difficulties.

A Spanish study found some improvement in thinking abilities among people with Down's syndrome who took a supplement of green tea extract, and also had training, for a year.

The study involved comparing the effects of the extract – gallocatechin-3-gallate (EGCG) – on cognitive abilities compared with a dummy treatment (placebo).

The study gave 43 adults with Down's EGCG and compared them with 41 adults with Down's given a placebo.

The researchers used 24 cognitive tests. They found improvements in three of the tests for the extract group.

These tests looked at visual memory, the ability to control inhibitions when instructed to, and the ability to carry out everyday living tasks. Results for the other 21 tests were not significantly different between the groups.

Brain scans of 10 people from each group seemed to show more nerve cell connectivity in the group who took the extract.

However, too few people were given brain scans for us to be sure this result is not down to chance.

While a few cups of green tea a day is unlikely to cause any problems, experts have warned that people living with Down's syndrome, or their carers, should not "self-medicate" with green tea extract.

Different varieties contain different concentrations of EGCG, which may affect the heart at some concentrations.

This research is certainly worth further investigation, as at present there are no pharmacological treatments specifically designed for people living with Down's.

Where did the story come from?

The study was carried out by researchers from the University Pompeu Fabra, Autonomous University of Barcelona, Hospital del Mar Medical Research Institute and CIBER Mental Health, Polytechnic University of Catalonia, University Paris Diderot, University of Paris, Jerome Lejeune, and the Fundacio Catalana Sindrome de Down.

It was funded by the Jerome Lejeune Foundation, Instituto de Salud Carlos III, MINECO and Generalitat de Catalunya.

The study was published in the peer-reviewed journal, The Lancet Neurology.

The reports in the Mail Online, The Telegraph and The Independent take quite a while to mention that most of the test results showed no difference between the groups.

However, they did include quotes from experts making it clear further research and larger trials are needed.

What kind of research was this?

This was a double-blind randomised controlled trial (RCT), which is the best way of telling whether a treatment works.

However, it was relatively small (84 people) and only lasted one year, so larger studies with longer follow-up are needed to see if the results last.

What did the research involve?

People with Down's syndrome aged 16 to 34 were divided randomly into two groups.

Everyone was given online thinking and memory training three times a week for a year. Half the people in the group took capsules of EGCG, while half took placebo.

The participants had tests of their thinking and behavioural abilities at the start, after six months and 12 months, then six months after the study ended. Researchers compared the results between the groups.

The study used tests of thinking and memory developed to test cognitive abilities, including:

  • attention
  • reaction speeds
  • memory
  • ability to make decisions
  • use of language
  • ability to adapt to different circumstances
  • ability to carry out everyday functions and the resulting effects on quality of life

These tests are still under development in relation to their ability to measure changes in ability among people with Down's syndrome.

Researchers compared the results of the tests between the two groups to see whether EGCG had an effect over and above any effects seen from thinking and memory training.

As well as the tests of thinking and behaviour, a sub-group in the study had brain scans using functional MRI – a type of brain scan that can track real-time activity inside the brain – and transcranial magnetic stimulation to measure connectivity patterns between brain cells.

However, these tests were done to explore what might be happening in the brain and were not designed to show a difference between groups.

What were the basic results?

For most of the tests (21 of 24) there were no differences between the groups.

However, in three tests people who'd taken EGCG did better. This improvement lasted for six months after the study ended.

These were:

  • remembering and recognising patterns
  • inhibitory control – the ability to override instinct to follow instructions; for example; in this test, to say "cat" when shown a picture of a dog, and vice versa
  • ability to carry out everyday living tasks (adaptive behaviour)

It is not clear how much difference these improvements made to people's everyday lives. We don't know whether the differences in scores between the EGCG and placebo groups were big enough to be noticeable.

People who took the green tea extract did not have an improvement in their overall quality of life, compared with those taking placebo.

How did the researchers interpret the results?

The researchers said that, "Even though the effects of EGCG and cognitive training on cognitive function were small and of subclinical magnitude, they were accompanied by a positive functional change on adaptive behaviour, with an absence of relevant negative side effects."

In other words, they admit most of the tests showed little difference, and those differences they did find might not be important.

But the researchers said the improvement in people's ability to carry out everyday tasks and the apparent lack of side effects means the benefits are "substantial".

They say their exploratory brain scans showed EGCG might affect the brain's ability to make connections between brain cells, and this could be linked to the extract's effect in inhibiting an enzyme called DYRKIA, which is overexpressed in people with Down's syndrome.


This is an interesting, but early-stage, study into a treatment that might help people with Down's syndrome cope better with everyday life.

However, the study does not provide conclusive evidence that green tea extract makes a big difference to people's thinking, memory or behaviour.

Down's syndrome is a complex condition caused by an extra copy of a chromosome in someone's genes. It's not usually inherited. It has a range of effects, which include learning disabilities of differing degrees of seriousness.

While early intensive training in childhood may help, there are no approved treatments for adults to improve learning disabilities.

Research into treatments or training that can help people with Down's syndrome to live a more independent life is very welcome.

This study has a number of limitations. The researchers looked at a wide range of test results, only a few of which were positive.

Carrying out multiple tests increases the risk that some results may be positive simply because of chance.

Also, the tests for changes in cognitive function in this group of people are not yet established, so we can't be sure they are a reliable way of measuring cognitive improvements.

Bigger, longer-running studies might help establish whether green tea extract really is useful alongside cognitive training for people with Down's syndrome.

We also need to see toxicity studies to be sure that high levels of green tea extract are safe for adults and children with this condition.

While a few cups of green tea shouldn't pose any threat to health, there have been warnings that people living with Down's syndrome, or their carers, should not "self-medicate" with green tea extract because of this uncertainty.  

Links To The Headlines

Green tea could be used to treat brain issues caused by Down's Syndrome, researchers say. The Independent, June 7 2016

Could people with Down's syndrome benefit from GREEN TEA? Drink shown to improve memory, speaking and quality of life. Mail Online, June 7 2016

Down's syndrome 'can be treated with green tea'. The Daily Telegraph, June 7 2016

Links To Science

de la Torre, de Sola S, Hernandez G, et al. Safety and efficacy of cognitive training plus epigallocatechin-3-gallate in young adults with Down's syndrome (TESDAD): a double-blind, randomised, placebo-controlled, phase 2 trial. The Lancet Neurology. Published online June 7 2016

Categories: NHS Choices

Depression blood test could lead to personalised treatments

Tue, 07/06/2016 - 18:30

"UK scientists have developed a blood test to help doctors pick the best drug for patients with depression," BBC News reports, somewhat prematurely.

It is currently unproven whether such a test, based on measuring inflammation, would improve treatment outcomes.

Previous research has suggested high levels of inflammation – which is not just a reaction to infection, but can also be caused by stress – may impair the beneficial effects of antidepressants.

Researchers screened blood samples from people with depression who had, and had not, responded well to antidepressant medicines in the hope of identifying molecules associated with inflammation and drug response.

They then used this information for a second group to see if they could predict who would and wouldn't respond to treatment with antidepressants.

A significant proportion of people were correctly identified as responders and non-responders, which is a big step forward compared with current practices.

But the test also missed 39-43% of non-responders, meaning they would continue to receive antidepressant treatment that is unlikely to work for them.

One of the study's limitations is its size. It was based on less than 200 people with depression, not nearly enough to draw any concrete conclusions about whether it works well in most people with depression.

The study also only looked at drug treatments, and did not assess talking therapies such as cognitive behavioural therapy.

This approach certainly seems to be a step in the right direction, but it needs refinement before personalised treatments for depression can be practised with confidence.

Where did the story come from?

The study was led by researchers from King's College London in the UK.

It was funded by the Medical Research Council, South London and Maudsley NHS Foundation Trust, King's College London, and the European Commission.

One of the study authors declared a potential conflict of interest, having received funding from Johnson & Johnson for research into depression and inflammation, as well as speaker fees for Lundbeck.

They have also received research funding from a large consortia, which included Johnson & Johnson, GSK, Pfizer and Lundbeck.

The study was published in the peer-reviewed International Journal of Neuropsychopharmacology.

The research is open access, so it is free to read online or download as a PDF.

The UK media's coverage was generally accurate, but there was some room for improvement.

Describing current depression treatment as "trial and error" (The Daily Telegraph and BBC News) is perhaps unfair on doctors and patients, who are attempting to jointly work out the best way to treat a serious condition with the options at their disposal.

For example, doctors usually prescribe the least powerful antidepressant available that is the least likely to lead to troublesome side effects, given the person's current and past medical history.

However, the reporting does touch on the uncertainty this treatment approach currently involves, which the new approach hopes to improve.

Also, some of the tone of the BBC's reporting could give the impression that this blood test had led to proven successes in terms of improved outcomes, which is currently not the case.

What kind of research was this?

This laboratory study looked to develop a way of classifying people with depression into those likely or unlikely to respond to commonly used antidepressant medicines.

The research team says higher inflammation levels have been linked to poorer responses to antidepressants in several studies.

But researchers hadn't yet developed accurate or reliable ways to predict who would benefit from antidepressants, and who wouldn't, so they could try a different type of drug or a non-drug treatment.

Part of the problem is we don't fully understand the biology of depression, making it difficult to know which molecules or processes to target to develop a predictive test.

What did the research involve?

Researchers screened blood samples from people with depression who had, and had not, responded well to antidepressant medicines in the hope of identifying molecules that could distinguish the two groups.

The researchers didn't measure these molecules directly. Instead, they counted up the number of messenger RNA (mRNA) molecules in the blood – small strands of genetic material that carry instructions to build many biological molecules.

This, they said, gave a reliable and accurate measure of the levels of the immune messengers, and had the added benefit of being able to be detected accurately and reliably by a simple blood test sent to the lab.

Seventy-four people with major depression (at least moderate severity), most of whom were in their second episode of depression, had their mRNA analysed to identify potential predictive molecules, as well as cut-off points for responders and non-responders.

These people came from a randomised controlled trial comparing 12 weeks of treatment with the antidepressants escitalopram (a selective serotonin reuptake inhibitor, usually the first choice class of antidepressant) and nortriptyline (a tricyclic antidepressant, or TCA, an older class of antidepressant), so their response to these medicines was known.

Response was defined as a greater than 50% reduction in score on a standard depression rating scale (the Montgomery-Åsberg Depression Rating Scale, MADRS).

To make sure these initial test cut-offs were accurate, the researchers tested them in a second validation sample of 68 people with depression using the same methods to detect responders.

This group had only recently started to take antidepressants and took a wider range, including:

  • escitalopram (SSRI)
  • paroxetine (SSRI)
  • duloxetine (serotonin and noradrenaline reuptake inhibitors, SNRI)
  • venlafaxine (SNRI)
  • amitriptyline (TCA)
  • desipramine (a TCA not licensed in the UK)

Patients were excluded from this part of the investigation if they were taking antipsychotics or mood stabilising medication.

The main analysis quantified the accuracy of the newly developed test to identify responders and non-responders to antidepressant medicines.

This included taking into account background differences in mRNA expression, which varies naturally from person to person.

What were the basic results?

Across the two studies, between 66% and 69% of patients responded to antidepressants.

Researchers identified mRNA linked to macrophage migration inhibitory factor and interleukin-1ß as the most useful to identify responders and non-responders.

Using their first group of patients, the test found:

  • 100% of those classified as non-responders were true non-responders (positive predictive value 100%, 14 of 14) – in other words a positive test result is 100% accurate
  • 100% of responders were correctly identified as being responders (specificity 100%, 51 of 51), meaning nobody on effective treatment would be unnecessarily "stepped up" to more advanced treatment
  • about 22% of the group were identified as "intermediates", meaning they weren't responders or non-responders – they fell in the middle
  • the test missed 39% of non-responders, falsely categorising them as responders (negative predictive value 85%) – a negative test result is only 85% accurate; this group would continue to receive standard antidepressant treatment that is unlikely to work for them

Results were very similar in the second group. The top two measures remained at 100% and the test missed 43% of non-responders, falsely categorising them as responders (negative predictive value 82%). Around 38% were classified as intermediates.

The researchers found background levels of mRNA made little difference to the test accuracy. All that mattered was the absolute amount of mRNA for macrophage migration inhibitory factor and interleukin-1ß.

How did the researchers interpret the results?

The researchers concluded that, "The absolute numbers of MIF [macrophage migration inhibitory factor] and IL-1β [interleukin-1ß] mRNA molecules are both accurate and reliable predictors of antidepressant response, identifying, for the first time, an mRNA-based biomarker approach that is independent from local experimental settings and does not require 'relative' quantification using housekeeping genes."


This study shows how a new blood test in development can help identify people with depression who are most and least likely to benefit from antidepressants.

While promising, the test is far from perfect. For example, it missed 39-43% of non-responders, meaning these people would continue to receive standard antidepressant treatment that is unlikely to work for them.

A large proportion of patients (22-38%) also fell into the "intermediate" group who were neither responders nor non-responders, so the test wasn't too useful here.

This means there is a significant proportion of people with depression who would not necessarily benefit from this test.

However, we shouldn't be overly negative. A significant proportion of people were identified correctly as responders and non-responders, which is a big step forward on what happens today.

The study was based on less than 200 people with depression, far too few to conclude whether it works well in most people with depression.

Larger studies involving many hundreds, perhaps thousands, of people will be needed to establish this, and is the natural next step for this research.  

Links To The Headlines

New blood test targets depression. BBC News, June 7 2016

Blood test could identify people who will respond to antidepressants. The Guardian, June 7 2016

Simple blood test could stop doctors using 'trial and error' to prescribe antidepressants, scientists claim. The Daily Telegraph, June 7 2016

Depression patients 'could get personalised treatment thanks to new blood test'. Mail Online, June 7 2016

Links To Science

Cattaneo A, Ferrari C, Uher R, et al. Absolute Measurements of Macrophage Migration Inhibitory Factor and Interleukin-1-β mRNA Levels Accurately Predict Treatment Response in Depressed Patients. International Journal of Neuropsychopharmacology. Published online May 11 2016

Categories: NHS Choices

Women are more likely to suffer from anxiety than men

Tue, 07/06/2016 - 16:40

"Women twice as likely as men to experience anxiety, research finds," The Guardian reports. A new review that attempts to get a global snapshot of the prevalence of anxiety disorders identifies a number of vulnerable groups.

There are various types of anxiety disorder, but generally they involve feelings of unease, such as worry or fear, that can be mild or severe and affect daily life. Having an overwhelming sense of anxiety that "takes over your life" is described as having a generalised anxiety disorder.

There are many factors that can trigger an anxiety disorder, such as stress, physical conditions, genetic background and hormonal imbalances.

The researchers found that women, young people and those with other chronic diseases were disproportionally affected. Across countries, women were found to be twice as likely to be affected as men.
The researchers call for further research to be carried out on the illness, as well as investigating which type of interventions have the greatest benefit. There is also a need for further study of anxiety prevalence in developing and under-developed parts of the world, as there was a lack of representation.

Although feelings of anxiety at certain times are completely normal, you should see your GP if anxiety is affecting your daily life or causing you distress.


Where did the story come from?

The study was carried out by researchers from the University of Cambridge and Westminster City Council. It was funded by the UK National Institute for Health Research. The study was published in the peer-reviewed clinical journal Brain and Behavior. It is available on an open-access basis and is free to read online.

While the media coverage was generally accurate, both the Mail Online and The Times claimed that the reasons why younger women had higher levels of anxiety were down to many of them being working mothers. This claim seems to be based on opinions, rather than any hard evidence presented in the study.


What kind of research was this?

This was a systematic review that aimed to collate evidence from other systematic reviews which had explored the prevalence of anxiety, to describe the burden of disease across population subgroups.

As the researchers mention, anxiety disorders contribute to significant disability and impairment to quality of life, and are the most prevalent mental health conditions in Europe. They place increasing demand upon health services across the globe, and are recognised as important determinants of poor health. This is the first reported study to attempt to provide a comprehensive synthesis of the findings from reviews undertaken on the global burden of anxiety.

Systematic reviews are one of the highest levels of evidence, but they are only as good as the studies they contain. The included reviews varied widely in their methods, the studies they had included and populations examined. Due to this variation, the researchers did not attempt to carry out a meta-analysis of their findings. Instead, they report the findings across the individual reviews.


What did the research involve?

The researchers searched three literature databases up to May 2015 to identify systematic reviews and meta-analyses that had reported the burden of anxiety across the globe.

Reviews could have looked at any anxiety disorder, including generalised, social anxiety or obsessive compulsive disorder, and use any method to assess anxiety. The researchers specifically searched for reviews including individuals suffering from other medical or mental health conditions (chronic or infectious disease, psychiatric conditions, and addiction) as well as those from vulnerable populations. Reviews on the treatment of anxiety were excluded.

Two researchers assessed the quality of the reviews and eligibility for inclusion, and extracted data.

The reviews included studies of people of all ages, from young children to people of old age, with the overall number of studies and individual study sample sizes varying. The method of anxiety assessment also varied between studies, from structured and unstructured interviews to self-reported questionnaires.


What were the basic results?

Results from the 48 studies were gathered to describe the global distribution of anxiety disorders. The main results were as follows:

  • The general prevalence of anxiety disorders in healthy populations ranged from 3% to 25%.
  • Women were found to be twice as likely to be affected as men (female: male ratio of 1.9:1). This was consistently the case across different countries and co-existing health conditions.
  • Young adults under the age of 35 were also more often affected (2.5% to 9.1%).
  • Prevalence was found to be highest in North America (7.7%, 95% confidence interval [CI] 6.8 to 8.8) and in North Africa/Middle East (7.7%, 95% CI 6.0 to 10.0).
  • The lowest prevalence was found in East Asia (2.8%, 95% CI 2.2 to 3.4).

The prevalence was then described according to five common themes:

  • addiction
  • other mental and neurological disorders
  • chronic physical diseases
  • trauma
  • vulnerable population subgroups

They found that, compared to healthy populations, the prevalence was higher in individuals with chronic conditions, who had a prevalence ranging from 1.4% to 70%.


How did the researchers interpret the results?

The researchers concluded: "Despite epidemiologic advances in this field, important areas of research remain under- or unexplored. There is a need for further studies on the prevalence of anxiety disorders. These recommendations can serve to guide the research agenda, and most importantly, help develop tailored and timely interventions."



This systematic review of previously gathered data compiled evidence from 48 studies to describe the global prevalence of anxiety disorders, which are placing increasingly high demand upon health services across the globe. The review gives us a general picture of the prevalence of these conditions worldwide and notes several themes.

It found that anxiety disorders are common across all population groups, but women and young people seem to be disproportionally affected. Anxiety prevalence was also higher in individuals with chronic conditions, though it is not possible to say whether mental health problems could be a contributing factor or a consequence.

Reviews were assessed for eligibility against a validated quality assessment tool. However, the researchers highlight the large variability in the methods of the reviews and the studies they included, which makes comparison of prevalence figures between the studies difficult.

For example, there was wide variation between reviews in:

  • the overall number of studies they included and their sample sizes
  • the ages of participants, with some reviews looking at older individuals and some looking at children (aged 6+)
  • whether they were general population samples or those with specific physical or mental health conditions
  • the tools used to assess anxiety
  • whether they took account of other health, environmental or lifestyle factors

While this review is a useful indicator of the prevalence of anxiety disorders, it is unable to suggest causation – for example, why prevalence may be higher in women or younger adults. It is possible that this could be down to a complex interaction of biological and lifestyle factors. However, the direction of effect or the extent of influence of different factors remains unknown.

The researchers call for further research to be carried out on the course of the illness, as well as anxiety levels pre- and post-treatment. They also note the need for further study into developing and under-developed parts of the world, as there was a lack of representation of those areas, and for specific study into vulnerable subgroups of society.

Visit the NHS Choices Moodzone for more information about stress, anxiety and depression, and methods you can try to cope with and combat these feelings.  

Links To The Headlines

Women twice as likely as men to experience anxiety, research finds. The Guardian, June 6 2016

Women 'nearly twice as likely to have anxiety' as men. BBC News, June 6 2016

Women twice as likely to worry than men. The Independent, June 6 2016

Women are almost TWICE as likely to suffer from anxiety as men. Daily Mirror, June 6 2016

Modern life is leaving women twice as likely to be stressed as men as they juggle work, family and children. Mail Online, June 6 2016

Women under 35 have it all — including anxiety disorders. The Times, June 6 2016 (subscription required)

Links To Science

Remes O, Brayne C, van der Linde R, Lafortune L. A systematic review of reviews on the prevalence of anxiety disorders in adult populations. Brain and Behavior. Published online June 5 2016

Categories: NHS Choices

Ten years of hormone breast cancer drugs 'may benefit some'

Mon, 06/06/2016 - 13:30

"Taking hormonal drugs for up to 15 years reduces the risk of breast cancers coming back," BBC News reports.

A new study looked at 1,918 postmenopausal women with what is known as oestrogen receptor-positive (or ER+) breast cancers – where cancer growth is stimulated by the hormone oestrogen.

A class of drugs known as aromatase inhibitors are often used in such cases, as they are able to reduce the production of oestrogen.

The women had previously responded well to a five-year course of hormone treatments.

They were randomised into two groups: either they took an aromatase inhibitor called letrozole for another five years, or they were given a dummy treatment (placebo).

Disease-free survival after five years was 95% in the treatment group and 91% in the placebo group.

Extended aromatase inhibitor treatment cut the risk of recurrent or new breast cancer development by about a third. 

Osteoporosis was the most significant side effect from extended treatment with letrozole.

However, there was no effect on overall survival, and no effect on disease-free survival when taking into account baseline differences between the participants.

It is hoped further evidence will be forthcoming to identify which women – in terms of characteristics, stage of breast cancer and prior treatment – may be most suited to this treatment, and for whom the benefits of prolonged treatment would outweigh the side effects.

Where did the story come from?

The study was carried out by researchers from the Avon International Breast Cancer Research Program at Massachusetts General Hospital Cancer Center and other institutions in the US.

Funding was provided by the Canadian Cancer Society Research Institute, the National Cancer Institute, the Canadian Cancer Trials Group, the ECOG-ACRIN Cancer Research Group, and Novartis Pharmaceuticals.

Several researchers declared conflicts of interest for serving on advisory boards for various pharmaceutical companies.

The study was published in the peer-reviewed journal, The New England Journal of Medicine, on an open access basis, so you can read it for free online.

The UK media reported on the study accurately, but many of the headlines included the phrase "women should stay on hormonal drugs for 10 years", or variations on it.

The researchers actually went out of their way to make the point that this study should not be taken as some sort of blanket recommendation for all women with ER+ breast cancer.

There was also apparent headline confusion on the BBC website over whether women should continue treatment for 10 or 15 years. This seems to come from the fact that most women had taken 5 years of tamoxifen prior to 10 years of an aromatase inhibitor.  

What kind of research was this?

This was a placebo-controlled randomised controlled trial that aimed to investigate the effects of extended treatment with an aromatase inhibitor (letrozole) in women with ER+ breast cancer.

ER+ means that the breast cancer cells have oestrogen receptors and the body's natural hormone is stimulating the cancer to grow. These cancers can be treated by hormone treatments, which can block this.

There are two types of hormone treatment – aromatase inhibitors, which are only given to postmenopausal women, and tamoxifen, which is most often used in premenopausal women, but can also be used in the treatment of postmenopausal women.

The problem is that even after treatment, there is always a risk the cancer will relapse or recur.

Hormone therapy regimens vary, depending on what treatment the person is having alongside it.

They can involve giving just an aromatase inhibitor for five years, or a combination of tamoxifen for five years and then an aromatase inhibitor for five years.

This placebo-controlled trial specifically aimed to look at the effect of giving an aromatase inhibitor for 10 years rather than 5, after any duration of previous treatment with tamoxifen.

What did the research involve?

The trial involved postmenopausal women with ER+ breast cancer who had received 4.5 to 6 years of treatment with an aromatase inhibitor.

In most women (two-thirds) this had been preceded by about five years of tamoxifen treatment.

A total of 1,918 women who were still disease-free after using aromatase inhibitor treatment were randomised to then receive the aromatase inhibitor letrozole or placebo for a further five years. Treatment started within six months of stopping their previous treatment.

Participants received yearly clinical assessments, including blood tests, mammography, bone scans, and assessment of drug side effects and quality of life.

The main outcome of interest was disease-free survival, defined as time from randomisation to breast cancer recurrence.

Other outcomes included overall survival, cancer development in the other breast, quality of life and long-term safety.

After five years, as the number of recurrence events in the placebo group was less than expected, the trial design was amended to look at the time that events occurred, rather than just looking at the number of events over continued follow-up time.

The duration of the study was five years, and the average follow-up period was 6.3 years.

What were the basic results?

The rate of cancer recurrence or new cancer development in the opposite breast was lower in the letrozole group, at 7%, compared with 10.2% of the placebo group.

The rate of disease recurrence specifically was 5.7% in the letrozole group versus 7.1% in the placebo group. Each year, around 0.21% of the letrozole group and 0.49% of the placebo group developed a new cancer in the other breast.

Five-year disease-free survival was higher in the letrozole group, at 95%, compared with 91% in the placebo group.

Letrozole reduced the risk of recurrence or development of cancer in the other breast by a third (hazard ratio [HR] 0.66, 95% confidence interval [CI] 0.48 to 0.91). 

There was no statistically significant difference when looking at overall survival, which was 90% in the letrozole group and 88% in the placebo group. Deaths were due to breast cancer, other primary cancers and cardiovascular disease.

Loss of bone density was a significantly more common side effect in the letrozole group, though few people in either group stopped treatment because of side effects. There was no difference between groups in terms of quality of life.

There was no significant difference between groups when adjusting for baseline characteristics and duration of prior aromatase inhibitor treatment.

How did the researchers interpret the results?

The researchers concluded that, "Extension of treatment with an aromatase inhibitor to 10 years resulted in significantly higher rates of disease-free survival and a lower incidence of [opposite] breast cancer than those with placebo, but the rate of overall survival was not higher with the aromatase inhibitor than with placebo." 


This trial suggests that extending the duration of aromatase inhibitor treatment for postmenopausal women to 10 years, rather than five, may reduce the risk of the cancer recurring or new cancer developing in the other breast.

The trial has many strengths, including:

  • a double-blind design, with neither participants nor the research team aware of allocation to treatment or placebo groups – this is regarded as the gold standard of assessing the effect of an intervention; adherence rates to five years were equivalent in both groups (62% in each), suggesting that participants were unaware of treatment 
  • stratified randomisation – this ensured baseline characteristics were balanced between the groups
  • a large sample size and prior power calculation – this ensured the researchers enrolled a sufficient number of people to detect a difference in survival between the groups 

However, there are points to bear in mind. There was no difference between groups when including the outcome of overall survival – this was seen only when comparing new or recurrent breast cancer rates.

There was also no significant difference between groups when taking into account baseline characteristics.

This suggests some women may be better suited to, or would gain more benefit from, prolonged aromatase inhibitor treatment than others.

The trial has only looked at disease-free survival up to five years. Though this was better in the treatment group, this is comparing women who had just stopped 10 years of treatment with an aromatase inhibitor with women who took an aromatase inhibitor for five years, and stopped five years ago.

We don't know the outcomes for the extended treatment group another 5 or 10 years down the line.

Extended treatment with an aromatase inhibitor may prolong disease-free survival, but this doesn't necessarily mean it would definitely prevent breast cancer ever coming back.

These were also a select group of postmenopausal women with ER+ breast cancer, the majority of whom had received about five years of tamoxifen before taking an aromatase inhibitor.

The results cannot be applied to all women with breast cancer, who may have different characteristics, types and stages of breast cancer, as well as different treatment regimens.

Overall, the results of this large and well-designed randomised controlled trial suggest that extended treatment with an aromatase inhibitor to 10 years may be suitable for some women.

However, the potential side effects should be balanced with the quality of life that could be had from this treatment.

The manufacturers of letrozole report menopausal-like side effects, such as hot flushes, increased sweating and fatigue, are very common, affecting more than 1 in 10 women.

It needs to be determined which women would be most suited to this regimen, and for whom the benefits would outweigh the side effects. Such information would allow women to make an informed choice about their treatment. 

Links To The Headlines

Breast cancer: Taking hormonal drugs for up to 15 years can reduce risk – study. BBC News, June 5 2016

Breast cancer drugs should be given for 10 years, study shows. The Guardian, June 5 2016

Breast cancer patients should continue taking drugs for longer to prevent it returning, experts say. Daily Mirror, June 5 2016

Breast cancer patients 'should stay on hormonal drugs for 10 years to slash risk of the disease returning'. Mail Online, June 5 2016

Links To Science

Goss PE, Ingle JN, Pritchard KI, et al. Extending Aromatase-Inhibitor Adjuvant Therapy to 10 Years. The New England Journal of Medicine. Published online June 5 2016

Categories: NHS Choices

'Friendly' virus repairs damaged liver cells (but only in mice)

Fri, 03/06/2016 - 14:30

"Have scientists found a cure for alcoholism?," the Mail Online asks, missing the point of the research entirely.

Researchers were able to improve liver damage in mice, but this does not amount to curing an addiction to alcohol.

The study showed it was possible to create "bespoke friendly" viruses to infect cells known as myofibroblasts, which are cells associated with tissue repair. The virus passed on instructions that transformed the myofibroblasts into healthy liver cells in mice who had fibrosis (scarring) of the liver, known as cirrhosis.

Not all the experiments in the mice worked, but in those that did, the transformed liver cells looked and behaved normally, replaced some of the diseased liver cells, and led to less liver scarring.

Researchers will now attempt to refine this technique before seeing if it works in humans.  

Right now, this technique is not available as a new treatment. It represents one of the earliest stages of treatment discovery and development, which can take decades from start to finish.

If you do have a lifestyle that increases your risk of liver disease, such as heavy alcohol consumption, being obese, or injecting drugs, you should ask your GP for a liver function test. The symptoms of liver disease often only occur once it is too late to undo the damage.

Taking action to reduce your risk before this happens could restore your liver back to good health.


Where did the story come from?

The study was carried out by researchers from The University of California and funded by grants from the US National Institutes of Health.

The study was published in the peer-reviewed science journal Cell – Stem Cell.

The Mail Online's reporting was poor, failing on three main points.

Firstly, it asked an inappropriate question in its headline – "Have scientists found a cure for alcoholism?". A cure, or at least a partial repair, of liver damage would not amount to a cure for alcohol addiction. The headline confused alcohol with its main health consequence – alcoholic liver disease. There are many other consequences of chronic alcohol misuse – be it social, financial or mental health-related.

Secondly, nowhere in the article (let alone in the headline) did it mention that the study was on mice, so readers might naturally assume it involved people.

Thirdly, there are other causes of liver disease aside from alcohol, such as obesity (non-alcoholic fatty liver disease) or infection with the hepatitis C virus. The mice studied didn't have alcohol-induced liver disease.


What kind of research was this?

This was a laboratory study investigating a potential new treatment approach for liver fibrosis.

Liver fibrosis is the scarring and demise of your liver, following repeated cell damage and inflammation. Fibrosis can have many causes, including viruses (like hepatitis B and C), alcohol misuse, and fatty liver disease.

Despite the liver's somewhat unique ability to recover and regenerate, when liver cells are repeatedly damaged, such as through sustained heavy alcohol use, they gradually die and the organ stops working. Part of the damage is the build-up of collagen, which causes scarring and restricts blood flow.

The poorly functioning liver and restricted blood flow causes symptoms including jaundice, weight loss, swelling of the abdomen, vomiting blood and, ultimately, death.

The only cure for severe liver scarring, where the liver loses most of its functioning ability (liver failure), is a liver transplant. But there are not enough organs to meet demand, so medical researchers are always looking for alternatives.


What did the research involve?

The researchers reprogrammed types of cells called myofibroblasts into liver cells by injecting reprogramming instructions, via a "designer virus", into mice with liver disease.

Myofibroblasts were chosen as the target, as they produce the excess collagen which causes scarring.

The researchers carefully analysed whether the reprogrammed cells behaved like normal liver cells in the lab and had similar DNA and protein profiles. They also tested whether once injected they were able to grow, repair and replace some or all of the liver damage.

Part of the challenge was devising a safe and effective way to deliver the reprogramming instructions to the mice myofibroblast cells. They used adeno-associated virus 6 (AAV6) vectors to act as delivery vehicles.

This involved taking the packaging of a virus and modifying it, so instead of infecting a mouse and causing disease, it infects the mouse and makes the modifications they wanted – in this case, turning myofibroblasts into liver cells. This involves replacing and modifying the virus DNA – that instructs the virus cell – with DNA encoding instructions you want.


What were the basic results?

The researchers overcame the delivery and reprogramming challenges to influence some cells to change from myofibroblasts into liver cells by injecting the reprogramming instructions into the bloodstreams of the mice using different AAV vectors.

Not all of the vectors worked. But in those that did, not only did some cells change, they appeared to function like normal liver cells, were able to grow and multiply, and reduced the amount of problematic collagen.

This partially alleviated two of the main causes of liver fibrosis – liver cell death and collagen build up – in mice with liver disease.


How did the researchers interpret the results?

The researchers concluded: "Our study establishes the feasibility of in vivo reprogramming of myofibroblasts into fully functional hepatocytes [liver cells] using AAV vectors, a gene delivery tool that proved to be safe and effective in clinical trials of liver-directed gene therapy".



This study showed it was possible to engineer and inject instructions that transform myofibroblasts into liver cells in mice with liver disease, which is quite a feat. Not all delivery mechanisms, called vectors, worked, but in those that did, the new liver cells looked normal, replaced some of the dying cells, and led to less damage due to collagen build up.

Despite the alcoholism-related headline, the mice did not have alcohol-induced liver damage – although this is a major cause of liver damage in people.

This study serves to prove this approach is feasible, and was successful in doing this. Researchers will now need to refine the technique before testing to see if it works in human trials.  

The good news is the vector delivery system has been used in human trials before – although not containing the same liver cell transformation message – so has a better chance than normal of working in people.

Right now this technique is not available as a new treatment. It represents one of the earliest types of treatment development, which can take decades from start to finish.

Currently the only cure for severe liver scarring is an organ transplant, but many die while waiting for a transplant as need far outstrips supply. If you are not on the register, you could save lives by joining the NHS Organ Donor Register today.

The liver is tough and can regenerate itself, but it can only take so much damage. Moderating your alcohol consumption, maintaining a healthy weight, and reducing your risk of contracting hepatitis C (mainly spread by injecting drugs), will do much to keep your liver healthy. 

Links To The Headlines

Have scientists found a CURE for alcoholism? New virus can 'repair the liver damage caused by drinking'. Mail Online, June 3 2016

Links To Science

Rezvani M, Español-Suñer R, Malato Y, et al. In Vivo Hepatic Reprogramming of Myofibroblasts with AAV Vectors as a Therapeutic Strategy for Liver Fibrosis. Cell Stem Cell. Published online June 2 2016

Categories: NHS Choices